THE  LIBRARY 

OF 

THE  UNIVERSITY 
OF  CALIFORNIA 

PRESENTED  BY 

PROF.  CHARLES  A.  KOFOID  AND 
MRS.  PRUDENCE  W.  KOFOID 


THE 


ORIGIN    OF    DISEASE, 

ESPECIALLY  OF 

DISEASE  RESULTING  FROM  INTRINSIC  AS  OPPOSED 
TO  EXTRINSIC  CAUSES. 


WITH 


CHAPTERS  ON  DIAGNOSIS,  PROGNOSIS,  AND  TREATMENT. 


BY 

ARTHUR  V.  MEIGS,  M.D., 

PHYSICIAN    TO    THE    PENNSYLVANIA    HOSPITAL. 


WITH  ONE  HUNDRED  AND  THIRTY-SEWN  ORIGINAL  ILLUSTRATIONS. 


PHILADELPHIA: 

J.  B.  LIPPINCOTT   COMPANY. 

LONDON :  6  HENRIETTA  STREET,  COVENT  GARDEN. 

1897. 


COPYRIGHT,  1897, 

BY 
J.  B.  LIPPINCOTT  COMPANY. 


K-R8 


L  \  lo 


y 


TO  THE   MEMOKY 

OF 

RICHARD    BRIGHT, 

AND  OF 

WILLIAM  WITHEY  GULL  AND  HENRY  GAWEN  BUTTON 

WHOSE  JOINT   LABORS   HAVE  SHOWN 

BRIGHT'S    DISEASE 

TO   BE   A   WIDE-SPREAD   PROCESS,    RATHER  THAN   A 
DISEASE   OF   THE   KIDNEYS, 

THIS  BOOK 

IS    IN   ADMIRATION   DEDICATED. 


PREFACE. 


MUCH  of  the  progress  of  medicine  in  the  past  fifty  years  has  been 
due  to  specialism.  Well-qualified  men  have  devoted  themselves  to 
restricted  fields,  and  important  discoveries  have  been  made  that  would 
not  have  been  possible  had  they  extended  their  labors  more  widely. 
The  advantages  of  specialism  are  patent ;  but  it  is  certain  that  a  wide 
divergence  of  knowledge  also  results  from  it,  and  that  facts  which  be- 
long together  are  often  observed  by  persons  whose  lines  of  research 
lead  them  so  far  apart  that  for  a  long  time  the  conclusion  remains 
undiscovered.  There  is  great  need  for  something  to  counterbalance 
this  inevitable  evil  result,  and  to  bring  together  the  facts  which  iso- 
lated are  useless.  The  relation  of  clinical  medicine  with  pathology 
is  obvious,  and  there  can  be  no  doubt  that  they  are  separated  to  the 
disadvantage  of  both.  Specialism  therefore  has  gone  sufficiently  far, 
if  not  already  too  far,  in  medicine,  and  it  is  time  that  something  be 
done  to  connect  the  various  disjointed  threads  of  knowledge,  the  true 
value  of  which  can  never  be  known  until  they  are  woven  into  a  com- 
plete whole.  Impressed  by  the  separation  of  clinical  medicine  from 
pathology,  I  have  endeavored  to  bring  them  nearer  together,  and  my 
book  is  the  result  of  that  effort. 

At  autopsies  in  hospital  practice  it  has  been  my  custom  to  retain 
for  microscopical  examination  portions  of  the  five  great  organs, — 
heart,  lung,  liver,  spleen,  and  kidney, — and  of  any  other  tissue  the 
appearance  of  which  seemed  to  indicate  disease.  The  habit  of  exam- 
ining with  the  microscope  portions  of  the  five  organs  named,  even  if 
no  disease  was  apparent  to  the  unaided  eye,  has  been  prolific  of  result. 
It  is  common  for  lesions  which  entirely  escape  the  closest  macroscopic 
investigation  to  be  revealed  by  the  microscope.  Thus  by  examining 
tissues  revealing  no  unhealthy  appearance,  the  beginnings  of  disease 
can  be  studied. 

It  is  often  difficult  to  determine  whether  an  unnatural  condition 
that  is  seen  with  the  microscope  is  due  to  post-mortem  change  or  bad 


vi  PREFACE. 

technique,  or  is  actually  disease.  This  difficulty  I  have  endeavored  to 
reduce  to  a  minimum  by  pursuing  a  uniform  method  of  fixation  of 
tissues  and  of  preparation  of  sections.  Small  pieces  of  all  tissues  to 
be  examined  with  the  microscope  were  cut  at  the  time  of  the  post- 
mortem examination  and  at  once  placed  in  seventy  per  cent,  alco- 
hol, which  was  frequently  changed  during  the  first  forty-eight  hours, 
except  in  the  case  of  nervous  tissues,  when  Muller's  fluid  (solution  of 
bichromate  of  potassium  and  sulphate  of  sodium)  was  used.  Paraffine 
has  been  the  embedding  material,  and  carmine  the  stain.  A  carmine 
solution  of  uniform  strength  was  used,  and  the  tissues  kept  in  it  for  a 
certain  length  of  time.  The  color  is  an  important  matter,  for  the 
condition  of  tissues  is  often  judged  by  the  way  in  which  they  take  the 
color  or  remain  unstained.  Besides  the  method  of  examination  that 
has  been  described,  others  have  been  used  when  the  occasion  seemed 
to  demand  it. 

The  pursuance  of  a  uniform  plan  of  examination  is  most  impor- 
tant, for  after  a  sufficient  degree  of  experience  has  been  attained  it  is 
possible  to  make  a  reasonably  certain  distinction  between  disease  and 
changes  due  to  other  causes. 

In  elaborating  my  work  it  was  necessary  to  make  the  argument  as 
complete  as  possible,  and  no  great  number  of  quotations  could  be 
included,  nor  many  references.  This  may  sometimes  make  it  seem  as 
if  it  is  intended  to  claim  as  my  own  observations  that  were  made  by 
others,  which  is  not  my  intention ;  all  that  is  claimed  being  that  the 
general  thread  of  the  argument  and  the  conclusions  are  my  own. 
These  are  necessarily  based,  to  a  great  extent,  upon  the  observations 
of  others,  although  there  are  a  good  many  facts  that  are  new  and  have 
not  been  previously  recorded,  especially  in.  regard  to  microscopical 
pathology. 

The  one  hundred  and  thirty-seven  illustrations  are  all  original,  and 
were  made  by  Mr.  Hermann  Faber  and  Mr.  Erwin  F.  Faber.  It 
would  be  impossible  to  exaggerate  the  faithfulness  and  skill  with 
which  they  have  performed  their  work.  All  but  one  of  the  pen- 
drawings  are  by  Mr.  Erwin  F.  Faber,  and  the  etchings  on  steel  are 
partly  by  one  and  partly  by  the  other  of  the  artists.  The  sections  of 
tissues  are,  with  two  exceptions,  my  own  preparations.  The  draw- 
ings were  made  with  the  camera  lucida,  the  outlines,  dimensions, 
and  relations  of  parts  being  thus  kept  true  to  nature.  With  each 
picture  is  a  scale,  magnified  to  the  same  extent  as  the  tissue,  which 
enables  any  one  to  ascertain  the  enlargement.  The  method,  so  far  as 


PREFACE.  vii 

concerns  the  etchings,  has  probably  been  seldom  if  ever  previously 
employed.  The  reflection  of  the  magnified  object  was  thrown  by  the 
camera  lucida  upon  the  steel  plate  and  traced  directly  with  the  needle 
by  the  etcher,  thus  obviating  the  necessity  for  the  intermediate  sketch 
which  is  ordinarily  used  in  etching.  For  accuracy  this  method  can- 
not be  surpassed. 

In  the  Pennsylvania  Hospital,  with  which  institution  I  have  been 
connected  almost  continuously  in  one  capacity  or  another  as  physician 
for  twenty-five  years,  I  have  enjoyed  almost  unlimited  opportunity  for 
study.  Only  those  who  have  been  associated  with  hospitals  can  appre- 
ciate the  gratitude  and  loyalty  felt  by  a  physician  for  the  institution 
which  has  rendered  him  this  invaluable  service. 

Throughout  my  work,  from  its  conception  to  the  printing  of  the 
last  page,  I  have  been  aided  by  my  friend  Dr.  Harvey  Shoemaker. 
Beginning  as  my  assistant  in  the  hospital,  he  has  continued  to  afford 
me  help  at  every  stage  in  the  construction  of  my  work.  I  owe  more 
than  I  can  express  to  his  kind  sympathy  and  good  advice. 

This  preface  must  not  be  closed  without  including  an  acknow- 
ledgment of  the  services  of  Mr.  Joseph  McCreery.  Through  his 
learning  and  by  his  fidelity  in  reading  the  proof-sheets  he  has  elimi- 
nated many  errors  from  the  text. 

May  19,  1897. 


CONTENTS. 


CHAPTER    I.  PAGE 

INTRODUCTORY  ...............................       l 

CHAPTER    II. 
THE  DISEASE  OF  AGE  ..........................  •       8 


CHAPTER    III. 
THE  ORIGIN  OF  DISEASE    .........................      l8 

CHAPTER    IV. 
BLOOD-VESSELS  ..............................     35 

CHAPTER    V. 
THE  HEART   ...............................     63 

CHAPTER    VI. 
THE  LUNGS    ........................   •   ......     88 

CHAPTER    VII. 
THE  LIVER     ...............................    102 

CHAPTER    VIII. 
THE  SPLEEN  ...............................    Il6 

CHAPTER    IX. 
THE  STOMACH    ..............................    123 

CHAPTER    X. 
THE  INTESTINES    .............................    126 

CHAPTER    XL 

THE  KIDNEY  ...................   ............    '3° 

ix 


x  CONTENTS. 

CHAPTER    XII. 

PAGB 

THE  SPINAL  CORD    ............................    I55 

CHAPTER    XIII. 
DIAGNOSIS  IN  CHRONIC  DISEASE  ^ 


CHAPTER    XIV. 
PROGNOSIS  IN  CHRONIC  DISEASE  ...............  .200 


CHAPTER    XV. 
THE  TREATMENT  OF  CHRONIC  DISEASE 205 


LIST    OF    ILLUSTRATIONS. 


1.  Obliterative  Endarteritis  (Moderate  Thickening  of  Intima) 38 

2.  Obliterative  Endarteritis  (Great  Thickening  of  Intima) 38 

3.  Obliterative  Endarteritis  (Complete  Closure  of  the  Vessel) 38 

4.  Obliterative  Endarteritis  causing  Distortion  of  the  Calibre  of  the  Vessel  ....  40 

5.  Obliterative  Endarteritis  causing  Distortion  of  the  Calibre  of  the  Vessel  ....  40 

6.  An  Artery  Narrowed  at  its  Origin 42 

7.  Early  Stage  of  Endarteritis 42 

8.  Earliest  Stage  of  Endarteritis,  from  an  Infant 44 

9.  Endarteritis,  from  an  Infant 44 

10.  Obliterative  Endarteritis 44 

11.  Obliterative  Endarteritis 44 

12.  Radial  Artery  with  Thickened  Muscularis 44 

13.  Obliterative  Endarteritis  (Complete  Closure  of  the  Vessel) 46 

14.  Obliterative  Endarteritis 46 

15.  Developing  Blood- Vessels 46 

16.  Arteriole  in  New  Growth  in  the  Colon 46 

17.  Endarteritis  and  a  Minute  Vessel  in  the  Wall  of  the  Arteriole 46 

1 8.  Adherent  Pericardium  and  Complete  Obliteration  of  the  Pericardial  Sac,  and 

New  Blood- Vessels 50 

19.  New  Blood- Vessels 50 

20.  New  Blood- Vessels « 50 

21.  Developing  Blood- Vessel  in  a  Valve  of  the  Heart 52 

22.  Developing  Blood- Vessel  in  a  Valve  of  the  Heart 52 

23.  Endarteritis  with  Blood- Vessels  in  the  New  Growth 52 

24.  Vascularity  of  the  New  Growth  in  Endarteritis 52 

25.  Vascularity  of  the  New  Growth  in  Endarteritis 52 

26.  Developing  Capillary  in  New  Growth  of  the  Intima  of  an  Artery 54 

27.  Developing  Capillary  in  New  Growth  of  the  Intima  of  an  Artery 54 

28.  An  Atheromatous  and  Calcareous  Radial  Artery 54 

29.  An  Early  Stage  of  Arterial  Atheroma 54 

30.  An  Excrescence  upon  the  Inner  Surface  of  the  Aorta 56 

31.  Early  Stage  of  Aortic  Aneurism 56 

32.  Early  Stage  of  Aortic  Aneurism 56 

33.  Tubercular  Arteritis 58 

34.  Vein  and  Artery  showing  Thickening  of  the  Intima  and  General  Atheroma    .    .  60 

35.  Diseased  Vein 60 

36.  Thickened  and  Degenerated  Vena  Cava 60 

37.  Growths  in  the  Wall  of  a  Vein 60 

'xi 


xii  LIST   OF   ILLUSTRATIONS. 

FIG.  PAGE 

38.  Growths  in  the  Wall  of  a  Vein 60 

39.  Normal  Efferent  Capillaries  of  the  Heart 64 

40.  Capillaries  within  the  Muscular  Fibres  of  the  Heart 64 

41.  Diagram  showing  Disease  of  Capillaries  of  the  Heart 66 

42.  Distortion  and  Disease  of  the  Muscular  Fibres  of  the  Heart  with  Narrowing  of 

the  Capillaries 68 

43.  Fibroid  Heart  with  Distortion  of  the  Muscular  Fibres 68 

44.  Inflammation  causing  Condensation  of  the  Fat  Layer  of  the  Heart 68 

45.  Inflammation  causing  Condensation  of  the  Fat  Layer  of  the  Heart 68 

46.  Fatty  Infiltration  of  the  Heart 70 

47.  Fatty  Infiltration  of  the  Heart 70 

48.  Cystic  Degeneration  of  the  Muscular  Fibres  of  the  Heart 70 

49.  Cystic  Degeneration  of  the  Muscular  Fibres  of  the  Heart 70 

50.  Cystic  Degeneration  of  the  Muscular  Fibres  of  the  Heart 70 

51.  Cystic  Degeneration  of  the  Muscular  Fibres  of  the  Heart 70 

52.  Fibroid  Heart 70 

53.  Hollow  Muscular  Fibres  of  the  Heart 72 

54.  Attenuated  and  Degenerated  Muscular  Fibres  of  the  Heart 72 

55.  Attenuated  and  Degenerated  Muscular  Fibres  of  the  Heart 72 

56.  Attenuated  and  Degenerated  Heart  Muscle  with  Capillaries  within  the  Fibres    .  72 

57.  Capillaries  entering  Muscular  Fibres  and  ramifying  among  them 72 

58.  Cystic  Degeneration  of  the  Muscular  Fibres  of  the  Heart 72 

59.  Cystic  Degeneration  of  the  Heart 76 

60.  Cystic  Degeneration  of  the  Heart 76 

61.  Cystic  Degeneration  of  the  Heart   . 76 

62.  Cystic  Degeneration  of  the  Heart 76 

63.  Pulmonary  Emphysema 90 

64.  Pulmonary  Emphysema 90 

65.  Pulmonary  Emphysema  in  a  Young  Infant 90 

66.  Pulmonary  Emphysema  and  Fibrosis  in  a  Young   Man  Dead  of  Acute  Dis- 

ease    92 

67.  Fibroid  Surface  of  the  Lung 92 

68.  Fibroid  Lung 94 

69.  Fibroid  Lung 94 

70.  Growths  in  the  Wall  of  a  Lung  Cavity 96 

71.  Degeneration  of  the  Liver  commonly  called  Nutmeg  Liver 102 

72.  Nutmeg  Liver 102 

73.  Nutmeg  Liver 102 

74.  Cystic  Disease  of  the  Liver 104 

75.  Cystic  Disease  of  the  Liver 104 

76.  Cystic  Disease  of  the  Liver 104 

77.  Cystic  Disease  of  the  Liver 104 

78.  Cystic  Liver 106 

79.  Cystic  Liver 106 

80.  Cystic  Disease  of  the  Liver 108 

81.  Cystic  Disease  of  the  Liver 108 

82.  Retrogression  of  Liver  Tissue.     The  so-called  New  Bile-Ducts 108 

83.  Retrogression  of  Liver  Tissue 108 

84.  Cirrhosis  of  Liver HO 


LIST   OF   ILLUSTRATIONS.  xiii 


FIG. 

85.  Fibrosisof  the  Liver   .........................  no 

86.  Fibrosis  of  the  Liver  in  Scattered  Spots  ............   .....  112 

87.  Disarrangement  of  the  Cells  of  the  Liver  and  Fibrosis  ...........  114 

88.  Degeneration  of  Liver  Cells  ......................  114 

89.  Fibroma  of  the  Spleen     ........................  116 

90.  Small  Fibroma  of  the  Spleen     .....................  116 

91.  Fibroid  Spleen  .....................    .......  116 

92.  Fibrosis  of  the  Spleen  .........................  Il6 

93.  A  Folded  Spleen  ...........................  118 

94.  Cystic  Spleen    ............................  118 

95.  Cystic  Spleen    ............................  120 

96.  Cystic  Spleen    ............................  120 

97.  Cystic  Spleen    ............................  120 

98.  Cystic  Spleen    ............................  120 

99.  Cystic  Spleen    ............................  120 

100.  Cystic  Spleen    ............................  120 

101.  Small  Cavities  in  the  Spleen  ......................  122 

102.  Small  Cavities  in  the  Spleen  ......................  122 

103.  Degeneration  of  the  Stomach     .....................  124 

104.  Ulcer  of  the  Colon  showing  Amyloid  Deposit  ......    .........  126 

105.  Ulcer  of  the  Colon  showing  Amyloid  Deposit     ..............  126 

1  06.  Earliest  Stage  of  Contracted  Kidney    ..................  132 

107.  Arteriole  entering  the  Kidney  from  the  Capsule      .............  132 

108.  Small  Fibroid  Spot  in  the  Kidney  ....................  134 

109.  Fibroid  Kidney     ...........................  134 

no.  Fibroid  Kidney     ...........................  136 

in.  Fibroid  Kidney     ...........................  136 

112.  Fibroid  Kidney  (resembling  Pulmonary  Emphysema)     ...........  136 

113.  Fibroid  Kidney  (resembling  Pulmonary  Emphysema)    ...........  136 

114.  Contracted  Kidney  ..........................  138 

115.  Contracted  Kidney  ..........................  138 

1  1  6.  Renal  Tubule  compressed  by  Fibrosis  ..................  140 

117.  Calcareous  Deposit  in  the  Kidney  ....................  140 

118.  General  Renal  Fibrosis,  Fibrosis  of  the  Medullary  Portion,  and  a  Growth 

resembling  Cancer  .........................  142 

119.  Growth  in  the  Kidney  resembling  Cancer    ................  144 

120.  Fibroid  Kidney    ...........................  146 

121.  Shredded  and  Thickened  Capsule  of  Kidney  ...............  146 

122.  Renal  Cyst  without  Fibrous  Wall  ....................  148 

123.  Renal  Cyst  without  Fibrous  Wall  ....................  14$ 

124.  Renal  Cyst  with  Thick  Fibrous  Wall     ..................  148 

125.  Small  Renal  Cysts  and  Amyloid  Disease  .................  150 

126.  Amyloid  Arteriole  and  Malpighian  Bodies  of  the  Kidney     .........  150 

127.  Peripheral  Fibrosis  and  Enlarged  Solid  Central  Canal  of  the  Spinal  Cord  .    .    .  156 

128.  Cystic  Disease  of  the  Spinal  Cord     .....    ..............  158 

129.  Cystic  Disease,  Fibrosis,  and  Degeneration  of  the  Spinal  Cord    .......  158 

130.  Degeneration  of  the  Spinal  Cord  in  Heart  Disease     ............  160 

131.  Degeneration  of  a  Peripheral  Nerve  in  Heart  Disease  ...........  1  60 

132.  Fibrosis  of  the  Spinal  Cord  in  Bright's  Disease  ..............  160 


xiv  LIST   OF  ILLUSTRATIONS. 

FIG-  PAGE 

133.  Disintegration  of  the  Spinal  Cord  in  Bright' s  Disease Ioo 

134.  Dropsy,  Universal  Degeneration,  and  Enlarged   Solid   Central  Canal  of  the 

Spinal  Cord 162 

135.  Degeneration  of  the  White  Substance  of  the  Spinal  Cord 162 

136.  Enlarged  Solid  Central  Canal  containing  a  Blood- Vessel 164 

137.  Blood- Vessel  in  the  Enlarged  Solid  Central  Canal  of  the  Spinal  Cord    .  ,164 


THE  ORIGIN  OF  DISEASE. 


CHAPTER    I. 

INTRODUCTORY. 

IN  the  earlier  part  of  my  work  as  a  hospital  physician,  rinding 
myself  without  any  understanding  of  microscopical  pathology,  and 
with  but  an  ordinary  and  superficial  knowledge  of  the  gross  appear- 
ances of  disease,  the  results  of  my  labors  were  exceedingly  unsatis- 
factory and  disheartening.  The  portion  of  the  work  in  a  hospital 
ward  which  consumes  the  greatest  amount  of  time  is  diagnosis,  for 
after  that  is  once  made  prognosis  almost  speaks  for  itself,  and  treat- 
ment, although  the  most  important  part  of  the  science  of  medicine,  is 
in  most  cases  simple,  and  its  direction  takes  but  little  time,  if  it  is 
possible  to  feel  assured  in  the  diagnosis.  Ward  work  pursued  with 
little  understanding  of  gross  and  none  of  microscopical  pathology 
soon  became  so  unsatisfactory  to  me  that  it  was  insupportable.  The 
accepted  views  of  disease  lead  to  a  degree  of  precision  in  their  classi- 
fication that  accords  ill  with  the  lesions  found  if  the  study  of  cases 
is  pursued  beyond  the  field  of  clinical  medicine  into  pathology  and 
the  results  studied  as  a  whole.  Most  cases  are  named  with  precision 
as  being  disease  of  one  organ  or  another.  This  may  be  a  sufficiently 
good  way  for  the  pathologist  who  can  work  at  his  leisure  and  in  turn 
study  the  various  different  morbid  conditions  to  which  the  heart, 
kidney,  or  other  organ  is  subject,  for  it  is  unnecessary  at  the  moment 
that  he  should  consider  either  the  fact  that  in  most  cases  more  than 
one  organ  is  involved  or  the  relations  of  lesions  of  different  organs 
one  with  another.  For  the  hospital  physician,  however,  who  studies 
pathology  in  the  cases  he  fails  to  cure,  the  classification  of  disease  by 
single  organs  is  almost  useless. 

The  result  of  some  years'  study  in  a  hospital,  including  attendance 
at  the  post-mortem  examinations,  convinced  me  that  to  have  any  real 

i 


2  THE   ORIGIN   OF   DISEASE. 

grasp  upon  the  management  of  disease  it  is  absolutely  necessary  to 
be  equipped  with  sufficient  understanding  of  pathology  to  be  able  to 
follow  that  side  of  medicine.  Study  pursued  in  this  way,  in  private 
practice  and  in  the  wards  of  a  hospital,  followed,  whenever  the  oppor- 
tunity offered,  into  pathology,  has  resulted  in  the  conviction  that  many 
diseases  usually  considered  as  confined  to  one  organ  are  seldom  so 
confined,  for  there  are  lesions  of  other  organs  that  are  just  as  definite 
as  those  of  the  part  considered  to  be  the  seat  of  origin.  At  the  same 
time,  many  of  the  lesions  are  of  such  nature  as  to  render  it  certain  that 
they  existed  before  the  onset  of  the  fatal  attack.  This  is,  of  course, 
much  more  the  case  in  chronic  diseases  than  in  those  which  are  acute, 
and  especially  than  in  those  which  are  acute  and  certainly  of  extrinsic 
origin.  These  two  facts — the  multiplicity  of  lesions  throughout  the 
body  in  diseases  commonly  looked  upon  as  being  of  one  particular 
organ,  and  the  frequency  of  lesions  that  long  antedate  the  fatal  attack 
— are  of  the  very  greatest  importance.  They  point  to  a  mode  of 
origin  of  disease  which  at  the  present  day  does  not  receive  its  due 
share  of  attention. 

For  practical  purposes  of  discussion  all  diseases  may  be  divided 
into  two  classes, — those  of  extrinsic  and  those  of  intrinsic  origin. 
Types  of  the  former  are  small-pox  and  measles,  which  are  caused  by 
poisons  that  pass  from  one  body  to  another.  The  contagious  entity 
to  which  such  diseases  are  due  is  as  much  a  thing  apart  from  the 
human  organism  as  a  bullet  which  kills  a  man  shot  through  the  brain. 
The  fact  that  the  real  nature  of  such  poisons  is  absolutely  unknown, 
whether  they  are  solid,  gaseous,  or  of  some  composition  as  yet  be- 
yond our  understanding,  does  not  lessen  the  certainty  that  the  cause 
is  extrinsic.  As  a  type  of  disease  of  intrinsic  origin  may  be  men- 
tioned the  formation  of  cysts  in  the  kidney,  which  is  so  common  a 
process  in  the  aged  and  in  those  suffering  with  contracted  kidney. 
It  is  the  result  of  abnormal  action  on  the  part  of  the  organism,  and  is 
entirely  independent  of  the  direct  action  of  any  extraneous  cause. 

That  the  causes  of  disease  are  so  divided  into  two  classes  no  one 
will  deny,  for  it  is  self-evident  to  all  who  have  reflected  upon  the 
subject.  Although  it  is  easy  to  recognize  types  of  the  extremes  of 
the  two  classes,  it  is  often  difficult  or  impossible  to  decide  how  to 
classify  individual  diseases,  for  with  disease,  as  with  almost  everything 
else  in  nature,  there  are  no  abrupt  lines.  Every  known  disease  has  a 
place  somewhere  on  the  long  stretch  that  reaches  between  those  cer- 
tainly of  extrinsic  and  those  of  purely  intrinsic  origin.  In  the  middle, 


INTRODUCTION.  3 

however,  between  the  two  extremes,  there  exist  diseases  which  un- 
doubtedly have  their  origin  in  a  combination  of  both  extrinsic  and 
intrinsic  causes.  Many  others  exist  whose  mode  of  origin  as  yet  re- 
mains unknown  or  is  in  dispute,  it  being  sometimes  said  that  they 
arise  from  the  action  of  a  poison,  or,  again,  that  they  are  the  result  of 
misdirected  growth  or  of  degeneration. 

Disease  should  be  looked  upon  as  a  complete  whole  composed 
of  very  heterogeneous  elements.  The  differences  of  these  elements 
at  the  extremes  are  radical  and  easily  recognized,  but  in  the  ordering 
of  diseases  Nature  has  followed  her  usual  plan  and  drawn  no  lines  to 
separate  them  into  sharply  defined  classes.  At  one  end  the  diseases 
of  positively  extrinsic  origin  are  shaded  toward  those  which  arise 
from  within,  owing  to  the  poisons  being  more  and  more  subtle  in  their 
action,  until  finally  it  becomes  impossible  to  ascertain  whether  there 
is  any  extraneous  cause  working  to  produce  a  particular  condition. 
At  the  other  end,  from  diseases  certainly  of  intrinsic  origin  we  reach 
gradually  others  which  are  complicated  by  the  operation  of  external 
causes  until  they,  too,  can  no  longer  be  satisfactorily  classified.  Thus, 
from  the  two  extremes  of  disease  of  extrinsic  and  of  purely  intrinsic 
origin  both  approach  a  common  centre,  becoming  gradually  in  their 
progress  more  and  more  alike,  until  finally  all  distinction  is  lost  and 
there  are  found  to  be  many  diseases  which  owe  their  existence  to  the 
double  action  of  causes  acting  from  without  and  from  within.  Such 
a  division  is  a  natural  one^for  it  is  certain  that  much  disease  is  due  to 
causes  external  to  the  organism,  and  it  is  equally  sure  that  mere  age 
will  produce  decay  and  degeneration,  for  the  very  rocks  disintegrate 
with  the  passage  of  time.  The  division  also  is  sufficiently  compre- 
hensive to  include  all  diseases.  It  must  be  confessed,  however,  that 
it  is  often  impossible  to  decide  where  between  the  two  extremes  par- 
ticular forms  shall  be  placed.  No  classifications  used  by  naturalists 
are  complete,  for  all  of  them  can  be  shown  to  be  imperfect,  if  not 
actually  unreasonable,  in  some  particular,  but  if  they  afford  us  a  means 
to  place  collections  of  abstract  or  concrete  things  in  an  orderly  man- 
ner for  use,  their  purpose  has  been  served,  and  they  may  remain  until 
superseded  by  something  better.  Even  the  division  of  disease  into  two 
classes  is  in  some  respects  imperfect,  for  the  causes  of  disease,  as  well 
as  the  diseases  themselves,  cannot  be  sharply  divided,  and  there  is  a 
middle  ground  for  doubt  or  dispute.  If  a  man  is  struck  upon  the  head 
with  a  hammer,  the  result  is  degeneration  or  destruction  of  the  part 
injured.  Is  the  cause  here  an  extrinsic  or  an  intrinsic  one  ?  There 


4  THE   ORIGIN   OF   DISEASE. 

has  been  nothing  of  the  influence  of  a  poison  to  produce  the  result, 
nor  could  it  be  charged  to  any  abnormal  action  of  the  organism  itself. 
The  state  of  the  atmosphere,  also,  often  operates  to  the  production  of 
disease.  In  this  case  the  mode  of  causation  is  even  more  complicated 
and  impossible  of  definite  explanation,  for  besides  the  capability  of 
the  atmosphere  to  produce  results  similar  to  those  of  a  blow,  as,  for 
instance,  the  effects  of  sufficiently  low  and  high  temperatures,  it  is  well 
known  that  the  air  often  carries  in  it  both  solids  and  liquids  which 
can  be  compared  only  to  poisons  in  their  injurious  effects.  When 
the  atmosphere  does  cause  disease  it  is  often  impossible  to  ascertain 
in  which  of  these  two  ways  the  result  has  been  brought  about.  The 
results  of  an  injury  like  a  blow,  or  the  harm  done  by  atmospheric 
conditions,  could  not  be  thought  to  be  caused  by  a  poison  or  to  be 
due  to  any  disordered  action  of  the  bodily  mechanism,  but  the  con- 
dition of  the  tissues  that  they  produce  is  much  more  like  what  results 
from  the  passage  of  time  than  like  the  ordinary  effects  of  poisons. 

My  intention  is  not  to  write  a  complete  treatise  upon  the  causa- 
tion of  disease,  but  only  to  describe  and  comment  upon  certain  obser- 
vations. What  has  already  been  said  has  been  for  the  purpose  of  ex- 
pressing in  brief  outline  views  which  are  universally  held  in  regard  to 
the  origin  of  disease,  avoiding  everything  in  regard  to  which  there 
might  be  controversy.  My  observations  have  led  me  to  believe  that 
many  diseases  originate  in  a  manner  different  from  that  commonly  sup- 
posed, and  that  there  is  often  a  connection  between  morbid  processes 
which  are  ordinarily  thought  to  be  unrelated.  The  sources  of  these 
observations  have  been  three, — private  practice,  ward  work  in  a  gen- 
eral hospital,  and  the  study  of  pathology. 

Private  practice  renders  possible  the  study  of  individual  cases  for 
many  years  continuously.  The  antecedent  period,  the  beginning  of 
disease,  its  progress  and  end,  may  all  be  followed.  If  the  end  is  death 
there  is  sometimes  also  the  opportunity  to  study  pathology,  and  under 
such  circumstances  is  obtained  the  most  complete  knowledge  of  a 
disease  that  it  is  possible  to  have.  In  private  practice  it  is  occasionally 
seen  that  chronic  diseases  usually  supposed  always  to  terminate  fatally 
may  last  for  many  years  and  finally  be  recovered  from,  or,  at  any  rate, 
the  patient  continue  in  such  good  general  health  that  for  all  practical 
purposes  he  may  be  considered  to  be  well.  This  is  especially  common 
in  cases  of  chronic  lung  disease  of  such  nature  that  it  is  impossible  to 
say  they  are  not  tubercular,  and  in  affections  of  the  kidney  which 
have  been  called  Bright's  disease,  and  which  a  few  years  ago  it  was 


INTRODUCTION.  5 

thought  always  proved  fatal  in  about  two  years.  The  largest  private 
practice,  however,  yields  but  a  small  field  for  the  study  of  clinical 
phenomena  in  comparison  with  what  is  obtained  in  the  wards  of 
hospitals.  In  them  are  grouped  vast  numbers  of  cases,  the  greatest 
portion  of  which  are  of  serious  nature,  for  but  few  persons  suffering 
with  the  more  trivial  ailments  and  diseases  find  their  way  into  hos- 
pitals. Besides,  the  patients  in  hospital  wards  are  almost  universally 
of  the  lower  classes,  and  in  such  people  all  diseases  which  tend  to 
recur  are  liable  to  be  of  more  severe  form  and  of  more  rapid  recur- 
rence than  among  those  of  the  better  class.  The  lower  classes  are 
so  much  exposed  to  physical  hardships,  and  owing  to  their  poverty 
are  so  often  forced  to  take  up  their  labor  again  after  an  attack  of  ill- 
ness before  having  had  sufficient  time  to  recover  fully,  that  their  con- 
dition as  seen  in  hospital  wards  presents  a  picture  which  has  no 
parallel  among  persons  of  the  better  class  who  are  not  subjected  to 
such  exposure.  In  them  diseases  of  the  heart,  lungs,  liver,  and  kid- 
neys, which  involve  the  existence  of  great  degrees  of  inflammation, 
recur  with  a  rapidity  and  virulence  that  are  surprising,  and  it  is  common 
for  persons  suffering  in  this  way  to  return  two  or  three  times  to  a 
hospital  within  a  short  period  and  die.  It  might  well  happen  to  an 
observer  of  disease  whose  studies  were  pursued  in  the  wards  of  a 
general  hospital,  where  the  number  of  chronic  cases  and  of  recurrent 
diseases  is  always  so  great,  to  exaggerate  the  importance  of  intrinsic 
causes,  which  play  so  large  a  part  under  those  circumstances,  and  to 
underestimate  the  effects  of  extrinsic  causes.  If  such  has  been  my 
error,  it  finds  its  excuse  in  the  natural  reaction  from  the  common  over- 
estimate of  the  importance  of  poisons  in  the  causation  of  disease. 
This  is  often  so  greatly  stretched  that,  if  no  semblance  of  an  extrinsic 
cause  for  a  particular  disease  can  be  found,  the  extremists  assume 
that  the  poison  must  exist  and  will  some  day  be  discovered,  and  then 
build  theories  upon  the  assumption. 

It  is  a  striking  fact  that  human  beings  are  much  more  liable  to  dis- 
ease during  early  life  and  when  they  have  become  old  than  in  the 
middle  period.  This  peculiarity  is  common  to  the  whole  organic 
kingdom,  being  the  rule  among  the  lower  animals  and  even  in  plants, 
just  as  with  human  beings,  who  represent  the  highest  type  of  organi- 
zation. The  reason  for  the  excessive  mortality  in  infancy  and  early 
life  is  in  a  way  easy  to  understand,  but,  on  the  other  hand,  no  single 
physical  cause  for  it  can  be  discovered  which  is  parallel  with  that 
which  explains  death  in  the  aged.  In  aged  beings  death  seems 


6  THE   ORIGIN   OF   DISEASE. 

natural,  for  all  the  parts  of  the  organism  become  worn  out,  but  with 
the  death  of  young  creatures  there  is  always  connected  a  feeling  of 
sadness,  as  though  some  injustice  had  been  done  and  with  a  better 
opportunity  the  calamity  might  have  been  avoided.  In  the  young 
decay  and  degeneration  seem  out  of  place.  Until  adult  life  is  reached 
the  tendency  is  entirely  the  other  way,  the  natural  inclination  being 
toward  perfection,  repair  is  easy,  and  growth  goes  on  until  the  full 
size  has  been  attained.  During  the  whole  period  of  growth  the 
capacity  to  overcome  the  ill  effects  of  any  injury  received  is  immense, 
for  so  long  as  growth  continues  new  tissue  is  produced,  and  this  is 
generally  uninfluenced  by  injuries  antecedent  to  its  existence.  In 
early  life  the  tissues  are  soft  and  succulent,  contrasting  strongly  with 
those  of  age,  which  are  dry  and  brittle.  They  are  prone  to  active 
inflammation,  which,  however,  is  seldom  of  long  duration  like  in- 
flammation in  the  old,  in  whom  it  tends  to  become  chronic.  The 
inelastic  and  hard  tissues  of  the  aged  are  disposed  when  once  inflamed 
to  continue  in  a  slow  or  latent  state  of  inflammation.  The  inclina- 
tion in  youth  is  toward  repair,  and  this  is  especially  strong  up  to  the 
time  when  full  size  is  attained,  and  the  natural  end  of  disease  or  in- 
flammation in  the  young  is  healing,  if  the  damage  is  not  irrepara- 
ble. In  considering,  however,  the  origin  of  disease,  it  must  not  be 
lost  sight  of  that  attacks  of  sickness  or  injuries  received  in  early 
life  may  often  lay  the  train  for  future  outbreaks.  It  is  not  rare  that 
the  seed  of  disease  is  planted  by  some  attack  in  infancy  or  childhood 
and  after  lying  dormant  for  years  develops  in  middle  life  or  old  age. 
This  peculiarity  will  be  fully  discussed  later.  The  diseases  of  ex- 
trinsic origin  flourish  during  early  life.  It  seems  as  if  the  nature  of 
the  tissues  invites  the  operation  of  all  the  extrinsic  causes  of  disease, 
and  especially  those  which  are  truly  contagious  are  readily  passed 
from  one  body  to  another.  On  the  other  hand,  the  fully  developed 
tissues  of  the  adult  period  are  comparatively  non-receptive,  and  in  old 
age  disease  of  extrinsic  origin  reaches  its  minimum. 

At  first  thought  it  would  seem  impossible  for  two  things  to  be 
farther  apart  or  less  related  to  each  other  than  youth  and  age.  They 
are  the  extremes  of  life,  and  under  natural  conditions,  if  no  obstruc- 
tions fall  in  the  way  of  physiological  development,  have  nothing  to  do 
with  each  other,  but  remain  always  far  apart.  Disease  accomplishes 
what  might  well  be  thought  impossible  :  it  forces  the  two  together,  and 
for  the  pathologist  there  is  produced  the  strange  paradox  of  the  com- 
mingling of  youth  with  age.  To  the  physiologist  such  an  assertion 


INTRODUCTION.  7 

may  seem  absurd,  and,  if  the  words  youth  and  age  are  held  strictly  to 
their  meanings  as  applied  to  the  length  of  life  of  beings,  to  be  impos- 
sible. If,  however,  the  subject  is  considered  from  the  stand-point  of 
pathology  and  the  condition  of  the  tissues  examined,  the  meaning 
of  the  assertion  that  youth  and  age  may  be  mingled  will  be  under- 
stood, and  it  will  be  perceived  that  disease  can  so  far  change  a  being 
young  in  years  as  to  produce  all  the  conditions  which  under  natural 
circumstances  are  found  only  in  the  old.  The  mingling  of  youth  with 
age  is  the  consequence  of  premature  age  in  youth,  and  not  of  anything 
like  a  postponement  of  the  natural  effects  of  time,  which  could  result 
only  in  something  like  immortality,  a  thing  which  in  the  present  state 
of  knowledge  seems  impossible.  This  subject  is  one  of  great  impor- 
tance, and  when  correctly  understood  it  will  be  seen  to  be  a  potent 
factor  in  the  origin  of  disease. 


CHAPTER    II. 

THE    DISEASE   OF   AGE. 

As  time  elapses  the  human  tissues  become  stiff  and  brittle,  fat 
accumulates,  and  there  is  a  great  increase  of  the  amount  of  fibrous 
tissue.  It  is,  however,  by  no  means  solely  the  number  of  years  a 
human  being  has  lived  that  makes  him  appear  most  nearly  typical  of 
youth  or  of  age.  Some  seem  born  to  live  long  lives  and  to  enjoy  a 
green  old  age,  looking  more  youthful  at  seventy  than  many  children 
prematurely  old  from  disease.  Such  children  become  wrinkled  and 
old-looking  while  yet  in  the  earliest  years  of  life,  and  die,  as  fruits 
dry  and  shrivel  and  fall  to  the  ground,  useless  before  maturity.  It  is 
not  intended  to  express  any  doubt  as  to  the  existence  of  a  healthy  old 
age,  or  to  assert  that  all  men  old  in  years  are  necessarily  diseased. 
Nevertheless,  the  pathological  changes  about  to  be  described  inevitably 
show  themselves  sooner  or  later  in  the  tissues  of  all  men  who  live  long 
enough  for  them  to  develop.  Otherwise,  if  the  various  accidental 
causes  of  death  could  be  escaped,  there  would  be  no  limit  to  the 
duration  of  life,  and  even  immortality  would  be  theoretically  possible. 
It  may  be  said  that  the  human  machine  must  wear  out  and  become 
incapable  of  further  work  within  one  hundred  years,  and  this  natural 
termination  of  the  life  of  man  is  as  inevitable  as  is  the  death  of  certain 
plants  after  they  have  performed  their  function  in  the  world  by 
producing  flowers  and  perfecting  seed.  In  man,  as  in  the  plant,  the 
period  of  extinction  is,  within  limits,  variable. 

The  period  at  which  the  body  begins  to  show  the  disease  of  age 
differs  greatly ;  often  it  is  premature,  owing  to  imperfections  or  to 
great  wear  and  tear  produced  by  dissipation,  excessive  labor,  or  some 
unhealthy  mode  of  living.  .In  making  post-mortem  examinations  one 
is  often  surprised  at  the  extremely  old  appearance  of  the  body  of  a 
child,  and  again  at  the  softness  and  pliability  and  generally  youthful 
appearances  presented  by  an  old  man.  It  is  well  known  that  at  birth, 
and  even  during  embryonic  life,  fibrous  tissue  exists  in  the  form  of 
tendons  and  other  necessary  portions  of  the  supporting  framework, 
and  that  a  moderate  amount  of  fat  is  also  to  be  found. 

The  question  of  the  significance  of  fat  is  one  in  regard  to  which 
8 


THE   DISEASE   OF  AGE.  9 

there  is  room  for  the  greatest  difference  of  opinion.  In  every  human 
body  there  is  more  or  less  adipose  tissue,  and  it  would  be  unreason- 
able to  say  that  fat  is  always  a  product  of  disease,  but  that  it  does 
often  accumulate  to  such  an  extent  as  to  be  pathological  is  undeniable. 
Every  physician  of  experience  has  met  with  cases  of  so-called  Bright's 
disease  in  the  course  of  which,  during  the  downward  progress  toward 
death,  either  an  enormous  accumulation  of  fat  developed  or  the  patient 
became  exceedingly  emaciated.  In  such  cases  albumen  and  casts  are 
present  in  the  urine,  and  the  degenerative  process  involves  in  greater 
or  less  degree  other  great  organs  as  well  as  the  kidneys.  When 
during  the  last  few  months  of  life  an  enormous  increase  of  fat  takes 
place,  the  patient  growing  in  weight  by  from  twenty  to  fifty  pounds 
and  still  becoming  weaker  and  more  short  of  breath  and  oppressed 
by  his  own  unwieldiness,  it  is  evident  that  this  growth  of  adipose 
tissue  which  insinuates  itself  into  every  space  and  fills  every  cavity  to 
bursting  is  morbid.  If  a  man  at  sixty  weighing  one  hundred  and 
seventy  pounds  begins  suddenly  to  gain  and  in  the  course  of  a  year 
or  two  reaches  two  hundred  and  ten,  meantime  becoming  visibly 
and  rapidly  older  in  body  and  mind,  it  is  only  reasonable  to  class 
the  condition  as  one  of  disease.  Such  a  change  during  the  latter 
part  of  life  is  not  rare,  and  persons  so  affected  become  mentally 
incapable  of  sustaining  that  which  was  formerly  easy  to  them.  The 
ordinary  affairs  of  life  become  burdensome,  they  fear  responsibility 
and  avoid  it,  and  when  unable  to  avoid  it  do  ill  that  which  formerly 
they  did  well.  In  function  the  digestion  becomes  weak  and  they  are 
prone  to  have  diarrhoea  or  to  be  constipated,  they  are  short  of  breath, 
and  frequently  take  cold,  or  are  very  rheumatic.  The  end  comes  with 
an  apoplectic  seizure,  dropsy,  subacute  pneumonia,  or  some  other 
apparently  acute  condition  whose  foundations  were  laid  in  the  invisible 
changes  that  occurred  in  the  organs  coincidently  with  and  as  a  part 
of  the  visible  increase  of  fat. 

This  sudden  accumulation  of  fat  during  the  latter  years  of  life  is 
difficult  to  comprehend,  and  at  the  present  time  it  is  impossible  to 
give  any  facts  showing  definitely  its  meaning ;  but  it  would  be  un- 
reasonable to  deny  that  it  constitutes  a  part  of  a  disease,  if  not  actually 
an  independent  disease  in  itself. 

The  morbid  increase  of  fibrous  tissue  is  one  of  the  most  interesting 
and  important  phenomena  presented  to  the  mind  of  the  discriminating 
pathologist.  The  tendons,  the  supporting  material  in  the  interstices 
of  the  kidneys  and  liver,  and  the  perivascular  connective  tissue  are 


io  THE   ORIGIN   OF   DISEASE. 

types  of  the  fibrous  tissues  known  to  histologists,  but  they  bear  little 
resemblance  to  that  which  forms  as  the  result  of  disease  in  the  organs 
and  elsewhere.  This  morbid  growth,  which  insinuates  itself  into  so 
many  places  where  it  has  no  natural  home,  is  hard,  dense,  and  un- 
yielding when  compared  with  the  soft  and  pliable  organs  in  which  it 
is  found ;  and  that  it  is  properly  named  fibrous  tissue  may  be  doubted, 
or  with  reason  denied  altogether. 

Many  arguments  might  be  adduced  favoring  the  belief  that  morbid 
fibrous  tissue  is  a  thing  entirely  different  from  healthy  fibrous  tissues, 
but,  as  it  would  be  impossible  now  to  bring  forward  facts  sufficient  to 
prove  the  accepted  opinions  incorrect,  it  does  not  seem  worth  while 
to  enter  into  a  very  full  discussion  of  the  subject. 

As  life  advances,  new  adaptations  and  changes  are  constantly  oc- 
curring, and  from  the  earliest  embryological  periods  to  the  most 
extreme  old  age  these  continue  without  any  periods  of  rest,  but  with 
the  greatest  apparent  variation  in  the  rate  of  progress.  Sometimes, 
as  already  said,  an  old  man  preserves  his  youthful  appearance,  and, 
again,  an  infant  may  caricature  the  appearance  of  age.  The  changes 
in  the  skeleton  have  been  studied  and  are  well  known.  The  skull 
grows  thick  and  increases  in  weight,  the  thigh-bones  lose  much  of 
the  cancellous  tissue,  are  lighter,  and  ill  adapted  to  bear  strain  and 
violence,  and  there  are  other  changes  that  are  well  known. 

An  interesting  feature  in  this  connection  is  the  increasing  com- 
plexity of  anatomical  structure  as  age  advances.  Nothing  could  be 
simpler  in  form  than  the  primitive  ovum,  and  yet  no  machine  has  ever 
been  constructed  which  is  so  complex  in  its  arrangement  as  the  adult 
human  organism.  The  increase  of  this  complexity  can  be  followed 
to  a  certain  extent,  and  the  reason  for  its  existence  can  be  easily  seen 
in  some  cases,  while  in  others  none  is  apparent.  As  an  instance  of 
the  first  may  be  mentioned  the  nervous  system,  which  begins  as  a 
shallow  furrow  upon  the  dorsal  surface  of  the  embryo.  It  then 
deepens  and  finally  closes  at  the  top,  thus  becoming  a  hollow  cylin- 
der. Later  the  walls  of  the  tube  increase  in  thickness  at  the  ex- 
pense of  the  cavity  until  a  solid  rod  is  formed,  and  meantime  it  has 
turned  and  folded  and  bent  itself  in  many  directions  and  at  many 
places  until  there  has  been  formed  from  so  simple  a  beginning  the 
marvellously  complex  human  brain  and  peripheral  nervous  system. 
The  reason  for  the  complexity  of  structure  here  exhibited  is  easy  to 
comprehend,  for  there  is  no  other  known  instance  in  nature  of  so 
complicated  an  organism  being  packed  in  so  small  a  space.  The 


THE   DISEASE   OF   AGE.  n 

second  proposition  is  illustrated  by  the  developmental  anatomy  of  the 
kidney.  It  is  well  known  that  the  Malpighian  bodies  lie  upon  both 
sides  of  the  bundles  of  straight  tubules  (the  pyramids  of  Ferrein) 
which  extend  outwardly  from  the  medullary  region  to  the  capsule. 
In  early  infancy  they  are  grouped  in  such  a  manner  as  to  present  the 
appearance  of  a  tree  with  its  branches,  with  fruit  hanging  at  their  ends. 
The  simplicity  and  beauty  of  the  arrangement  are  such  as  at  once  to 
catch  the  eye.  At  a  later  period,  however,  during  adult  life,  this 
arrangement  has  disappeared,  or  at  least  can  no  longer  be  seen,  and 
apparent  confusion  has  taken  the  place  of  the  former  simple  order. 
The  Malpighian  bodies  appear  to  have  increased  greatly  in  number, 
they  crowd  closely  upon  the  straight  tubules,  and  are  scattered  with- 
out apparent  order  throughout  the  labyrinthine  regions.  The  beau- 
tiful appearance  of  curving  branches  with  fruit  hanging  at  their  ends 
can  no  longer  be  seen. 

The  painful  joint-affection  of  the  aged  called  rheumatism,  in  the 
course  of  which  fibroid  material  increases  and  earthy  salts  are  de- 
posited in  and  around  the  articulations,  is  so  often  an  accompaniment 
of  age,  and  so  commonly  looked  upon  as  inevitable,  that  it  is  not 
unusual  to  hear  aged  people  express  thankfulness  at  their  freedom 
from  pain  if  they  chance  to  escape  this  particular  infliction.  This  so- 
called  rheumatism  of  the  aged,  so  far  as  the  anatomical  alteration 
of  the  joints  is  concerned,  appears  to  be  of  the  same  nature  as  the 
process  which  shows  itself  by  the  deposit  of  fibroid  material  in  the 
organs,  differing  only  in  the  locality  affected.  There  is  the  same 
slow  inflammation  with  alteration  of  the  part  invaded,  the  new  material 
deposited  being  useless,  if  its  presence  in  the  place  into  which  it  may 
have  intruded  does  not  become  actually  injurious.  If  this  view  is 
correct,  it  will  be  necessary  to  rearrange  somewhat  our  views  about 
rheumatism.  Either  that  which  has  been  called  rheumatism  in  the 
aged  is  not  rheumatism  at  all,  but  is  a  form  of  fibrosis  incident  to  age, 
or  else  all  varieties  of  rheumatism  are  of  this  nature,  and  are  to  be 
classed  as  species  of  degeneration.  Strange  as  such  a  doctrine  may 
at  first  sight  be  thought,  many  facts  might  be  adduced  which  lend  it 
strong  support.  The  acute  inflammatory  rheumatism  of  young  people 
does  not  at  a  cursory  view  present  any  resemblance  to  the  painful  and 
distorted  condition  of  the  joints  so  common  in  the  aged.  Acute 
rheumatism  is  peculiarly  the  disease  of  those  who  are  exposed  to 
dampness  and  wet,  notably  sailors,  and  it  is  at  first,  so  far  as  at  present 
known,  nothing  but  an  acute  inflammation  which  attacks  the  joints 


12  THE   ORIGIN   OF   DISEASE. 

and  the  heart.  One  of  its  marked  peculiarities  is  its  aptitude  to  recur, 
especially  if  the  mode  of  living  which  precipitated  the  first  attack  be 
continued.  Those  who  have  been  much  with  sailors  think  them 
short-lived  and  that  they  become  disabled  and  grow  old  early.  First 
attacks  of  rheumatism  in  young  people  are  most  commonly  of  the 
acute  variety,  and  when  the  attack  has  passed  away  the  individual  is 
left  as  well  and  active  as  ever.  Later  there  will  be  another  acute 
seizure,  or  perhaps  after  an  interval  of  perfect  health  an  attack  of  sub- 
acute  rheumatism  of  the  knees  or  ankles  or  other  joints.  During  the 
subacute  attacks  there  is  generally  no  fever,  and  no  disability  except 
that  caused  directly  by  the  local  affection  of  the  joints.  There  is 
none  of  the  general  bodily  sickness  and  prostration  which  are  invari- 
able accompaniments  of  acute  rheumatic  fever.  It  is  not  necessary  to 
describe  the  bodily  condition  of  a  rheumatic  old  man,  nor  is  it  needful 
to  say  that  all  possible  gradations  of  change  of  the  joints  occur,  from 
that  which  is  seen  in  the  most  acute  variety  of  rheumatic  fever  in  a 
young  sailor  to  the  so-called  rheumatism  of  the  octogenarian.  No 
one  has  ever  been  able  to  point  to  a  distinct  division  in  the  line  which 
has  at  one  of  its  ends  acute  rheumatism  and  at  the  other  chronic 
rheumatic  synovitis.  The  two  are  beyond  doubt  nearly  related  to 
each  other ;  they  are  at  most  only  different  species  of  the  same  genus. 
If  this  is  allowed,  and  it  is  conceded  that  the  rheumatism  of  the  aged 
is  a  degeneration,  a  form  of  fibrosis,  and  a  part  of  the  process  which 
occurs  in  the  organs  of  all  men  as  life  progresses,  then  it  follows 
that  acute  rheumatism  is  in  some  wise  of  the  same  nature.  There  is, 
therefore,  much  reason  to  think  that  all  rheumatism  is  degenerative, 
and  that  it  is  but  one  of  the  parts  of  that  which  has  been  called  the 
disease  of  age.  This  statement  may  seem  untenable,  if  not  almost 
absurd,  if  it  be  considered  from  the  side  of  our  experience  of  acute 
rheumatic  fever  alone.  More  careful  thought,  however,  establishes 
the  fact  that  chronic  synovitis  is  a  degeneration,  and  of  the  same 
nature  as  or  allied  to  fibrosis  of  the  organs;  and,  this  being  true, 
there  is  no  escape  from  the  conclusion  that  all  varieties  of  rheumatism 
belong  in  the  same  category,  however  unlike  the  extreme  youth  of 
the  disease,  which  is  acute  rheumatic  fever,  may  be  to  its  old  age, 
which  is  chronic  rheumatic  synovitis. 

The  influence  of  injuries  and  disease  upon  the  prospects  of  longevity 
is  a  problem  of  great  interest  and  importance.  It  is  probably  strictly 
true  that  no  morbid  process  involving  the  existence  of  inflammation 
ever  takes  place  without  leaving  the  part  attacked  in  a  more  or  less 


THE   DISEASE   OF  AGE.  13 

imperfect  condition.  Every  tissue  which  has  been  subjected  to  the 
malign  influence  of  inflammation,  beyond  the  earliest  and  slightest 
stage  of  congestion,  is  left  somewhat  scarred.  There  are  scars  of  all 
degrees,  from  the  slightest  condensation  of  tissue  which  can  be  dis- 
covered only  by  careful  microscopical  examination,  to  the  tough  and 
contracting  material  which  results  from  attacks  of  pleurisy.  It  does 
not  seem  to  be  overstepping  the  limits  of  truth  to  say  that  every  sick- 
ness which  occurs  during  life  bears  with  it  more  than  the  mere  danger 
of  the  moment,  and  is  an  injury,  which  must  leave  the  individual 
in  a  state  more  or  less  removed  from  physiological  perfection. 

Fibrosis,  which  is  the  growth  and  increase  of  morbid  fibroid  ma- 
terial, is  the  essential  pathological  change  incident  to  age :  it  is  the 
"  disease  of  age."  In  all  those  who  live  beyond  the  ordinary  term  of 
life,  excess  of  fibroid  tissue  develops,  and,  if  no  accidental  cause  of 
death  steps  in  to  close  the  scene,  this  degeneration  finally  reaches  a 
stage  when  life  can  no  longer  continue.  The  parallel  between  the  old 
man  and  the  ancient  tree  is  trite,  but  it  is  none  the  less  apt.  A  resem- 
blance can  be  conjured  up  in  almost  every  respect  between  the  bodily 
condition  of  the  aged  man  and  the  old  tree  with  its  hollow  trunk  and 
its  few  remaining  branches  of  rotten  wood,  which  is  brittle,  soft,  and 
lifeless,  without  sap,  and  unable  to  resist  strain. 

Among  all  the  diseases  received  into  the  modern  classifications 
there  is  none  which  comes  nearer  to  this  "  disease  of  age"  than  what 
has  long  been  named  Bright's  disease.  Bright's  disease  of  the  con- 
tracted form,  with  the  morbid  conditions  which  are  connected  with  it, 
is  identical  with  what  has  been  described  in  the  foregoing  pages. 
Contracted  kidney,  as  is  known  by  every  one,  is  associated  with  en- 
largement of  the  heart  and  disease  of  the  blood-vessels,  with  disease 
of  the  spinal  cord  and  brain,  with  bronchitis,  emphysema,  and  the 
slower  forms  of  pneumonia,  and  with  liver  disorders.  An  important 
lesion,  if  not  the  essential  one,  in  all  the  parts  involved  is  an  accumu- 
lation of  morbid  fibroid  tissue.  It  is  a  matter  of  common  knowledge 
that  old  people  are  prone  to  have  fibroid  and  cystic  kidneys,  and  that 
the  heart  is  larger  than  in  youth,  though  no  one  would  presume  to 
say  that  it  is  stronger.  The  stiffened  arteries  of  age  and  the  bron- 
chitis which  carries  with  it  emphysema  are  so  well  known  as  hardly 
to  need  mention.  All  human  beings,  then,  who  do  not  die  from  some 
other  cause  develop  fibrosis,  which  progresses  with  greater  or  less 
rapidity  until  the  organism  is  so  far  injured  that  something  must  give 
way ;  then  the  machine  stops.  This  is  as  true  of  man  as  it  is  of  the 


i4  THE   ORIGIN   OF   DISEASE. 

trees,  which  are  certain  to  grow  old  in  appearance  and  in  fact,  and 
with  them  age  constitutes  a  disease  which  produces  alterations  in 
many  respects  parallel  with  the  fibrosis  of  man. 

Age  in  mankind,  however,  if  it  is  to  be  looked  upon  as  a  disease, 
makes  its  appearance  at  no  fixed  period.  There  is  no  other  animal 
that  is  subjected  to  such  an  infinite  number  of  variations  in  its  methods 
of  living  as  is  man.  Man  lives  in  every  climate  where  any  mammal 
dwells  ;  his  houses  are  of  every  conceivable  gradation,  from  the  palaces 
of  Europe  and  the  East  to  huts  so  miserable  as  to  afford  less  shelter 
than  the  dwellings  of  many  of  the  lower  animals.  His  clothing  and 
work  and  the  food  and  drink  upon  which  he  subsists  could  not  be 
more  varied.  Owing  probably  to  his  widely  differing  environments, 
man  shows  the  greatest  variation  in  the  age  at  which  he  appears  to 
grow  old.  If  this  question  of  age  be  looked  at  from  a  point  of  view 
more  comprehensive  than  that  of  the  external  appearance  of  the  aged 
and  the  number  of  their  years  when  they  die,  if  it  be  examined  with 
the  aid  of  the  light  thrown  upon  it  by  the  science  of  pathology,  many 
things  of  great  interest  will  be  developed,  things  that  may  aid  in  build- 
ing up  knowledge  that  shall  enable  us  to  put  back  the  period  of  death 
even  farther  than  has  yet  been  possible.  The  opportunities  of  man  to 
disregard  the  rules  of  hygiene  and  to  indulge  in  practices  which  tend 
to  shorten  life  are  very  much  greater  than  those  of  any  of  the  lower 
animals.  No  one  of  the  lower  animals  cooks  its  food  or  partakes  of 
alcohol.  Man  does  both ;  he  eats  a  variety  of  food  and  an  amount 
ill  adapted  to  his  mode  of  life ;  he  eats  many  things  that  under  all 
circumstances  are  unwholesome ;  and  he  frequently  takes  a  quantity  of 
alcohol  quite  incompatible  with  the  continuance  of  good  health.  As 
a  consequence  he  is  liable  to  suffer  ills  that  have  no  parallel  either 
in  the  lower  animals  or  in  vegetable  life.  Fibrosis,  therefore,  that 
which  has  been  suggested  as  essentially  the  disease  of  age,  is  quite 
common  in  middle  age,  and  even  in  youth,  presenting,  so  far  as  the 
pathological  conditions  are  concerned,  exactly  the  same  appearances 
as  are  found  in  those  old  in  years.  It  is  apparently  the  result  of  dis- 
sipation or  overwork,  or  is  due  to  inherited  tendencies,  such  as  are 
transmitted  by  syphilis  and  tuberculosis,  or  to  any  combination  of 
these  causes.  Man,  then,  owing  to  his  mode  of  life,  may  die  at  any 
age,  even  in  youth,  of  a  disease  pathologically  the  same  as  that  which 
must  eventually  prove  fatal  to  all  men  who  escape  other  diseases  and 
accidental  causes  of  death.  As  a  result  of  inherited  tendencies,  its 
signs  often  appear  very  early,  probably  even  during  the  embryological 


THE   DISEASE    OF   AGE.  15 

period.  Bright's  disease  of  the  more  chronic  forms,  especially  con- 
tracted kidney,  with  the  wide  range  of  symptoms  and  many  patho- 
logical lesions  which  are  grouped  with  it,  is  the  type  of  the  disease  of 
age,  whose  essential  features  are  fibrosis  and  certain  changes  in  the 
blood-vessels.  It  is  impossible  at  present  to  determine  whether  the 
blood-vessel  changes  antedate  the  fibrosis  and  are  its  cause,  or  whether 
they  are  its  consequence ;  or,  on  the  other  hand,  whether  the  fact  that 
the  two  are  always  in  company  is  to  be  considered  as  a  mere  coin- 
cidence. The  last  possibility  is  in  the  highest  degree  improbable. 

In  his  book  "  Old  Age,"  George  Murray  Humphrey  *  attempts  to 
show  that  there  is  a  such  a  thing  as  physiological  death,  and  much 
is  adduced  which  is  very  interesting  and  instructive  concerning  the 
life  and  death  of  aged  people.  Some  idea  of  the  views  of  this  author 
may  be  had  from  the  following  (page  5  et  seq.) :  "  It  may  be  said,  in- 
deed, that  at  all  periods  of  life  the  healthy  and  well-working,  and 
especially  the  enduring,  quality  of  the  body  depends  upon  a  good 
adjustment,  a  good  balance,  of  the  several  parts;  and  it  is  upon  the 
well-ordered,  proportionately  or  developmentally  regulated  decline  in 
the  several  organs  that  the  stages  which  succeed  to  maturity  are 
safely  passed,  and  that  crown  of  physical  glory,  a  healthy  old  age, 
is  attained. 

"  A  time  comes  at  length  when,  in  the  course  of  the  descending 
developmental  processes,  the  several  components  of  the  machine, 
slowly  and  much,  though  equally,  weakened,  fail  to  answer  to  one 
another's  call,  which  is  also  weakened ;  a  time  when  the  nervous,  the 
circulatory,  and  the  respiratory  organs  have  not  force  enough  to  keep 
one  another  going ;  then  the  wheels  stop  rather  than  are  stopped,  and 
a  developmental  or  physiological  death  terminates  the  developmental 
or  physiological  decay.  The  old  man  who  had  gone  to  bed  apparently 
much  as  usual  is  found  dead  in  the  morning,  as  though  life's  engine 
had  been  unable  to  repair  itself  in  sleep  sufficiently  to  bear  the  with- 
drawal of  the  stimulus  of  wakefulness.  ... 

"  How  much  may  those  who  pass  gently  into  this  natural  and 
physiological  death  be  envied  by  the  many  sufferers  under  the  pro- 
tracted and  painful  pathological  processes  which  too  often  induce  a 
premature  extinction  of  life !  .  .  . 

"  Yet,  strange  and  paradoxical  as  it  may  seem,  this  gradual  natural 

*  Old  Age,  by  George  Murray  Humphrey,  M.D.,  F.R.S.,  Cambridge,  Macmillan  & 
Bowes,  1889.  Chapter  I.  is  the  Annual  Oration  delivered  before  the  Medical  Society  of 
London,  on  Monday,  May  4,  1885. 


16  THE   ORIGIN   OF   DISEASE. 

decay  and  death,  with  the  physiological  processes  which  bring  them 
about,  do  not  appear  to  present  themselves  in  the  ordinary  economy 
of  Nature,  but  to  be  dependent  upon  the  sheltering  influences  of  civil- 
ization for  the  opportunity  to  manifest  themselves  and  to  continue 
their  work.  For  the  needs  of  the  first  or  infantile  period  of  animal 
helplessness  Nature  has  made  a  sufficient  provision  in  the  parental 
instinct  which  protects  and  nurtures  the  young.  But  this  lasts  only 
so  long  as  the  requirement  for  it  exists.  It  ceases  as  soon  as  the 
young  animal  has  the  ability  to  help  itself;  and  it  does  not  return, 
and  is  not  supplemented  by  anything  of  its  kind.  It  gives  way  before 
that  struggle  for  existence  which  is  the  engenderer  of  selfishness,  which 
dominates  over  all  other  impulses  and  shuts  out  all  heed  for  the  worn 
and  weary,  for  the  feeble  and  the  decaying.  These,  being  unable  to 
help  themselves,  are  crushed  out  by  the  various  provisions  which 
Nature  makes  for  their  destruction.  The  good  result  of  this  great 
seeming  evil  is  that  all  in  the  natural,  or  primitive,  animal  world  is  in 
the  ascendant  to,  or  in  the  enjoyment  of,  bodily  perfection.  .  .  . 

"  The  same  with  disease.  It,  in  like  manner,  stops  itself.  Indeed, 
it  can  scarcely  be  said  to  be  allowed  to  enter  into  the  pure  realm  of 
Nature.  Sick  animals  are  not  there  provided  for,  have  no  abiding- 
place  there,  and  soon  perish ;  so  that  there  is  no  wasting  and  pining, 
no  lingering  fevers,  no  destroying  cancers,  no  decrepit  frames.  Neither 
the  bird  that  fails  to  elude  the  hawk,  nor  the  hawk  that  fails  to  seize 
the  bird,  can  long  continue  in  existence.  Each  animal  has  its  so-called 
enemy  ready  and  at  watch  to  deliver  it  from  feebleness  and  disease ; 
and  the  sudden  destruction  which  awaits  them  all,  without  fearful  pre- 
monition, and  with  little  pain, — this  killing  in  lieu  of  death, — instead 
of  being,  as  it  is  sometimes  regarded,  a  cruel  feature  in  Nature's  plan, 
is  a  happy  provision  for  deliverance  from  the  slower  death  which  in- 
creasing failure  or  progressive  disease  would  have  involved,  and  which 
civilization  entails." 

So  pleasing  is  the  picture  thus  drawn  that  one  is  disposed  at  first  to 
accept  it  as  correct  in  every  detail ;  but  a  consideration  of  the  hard 
facts  of  pathology  shows  that  some  modification  of  the  conclusions 
must  be  made.  That  there  must  be  a  well-ordered  and  regulated 
decline  in  the  several  organs,  in  order  safely  to  pass  the  period  which 
succeeds  maturity  and  before  old  age  is  attained,  is  a  just  statement 
of  an  important  fact,  and  at  this  stage  there  is  nothing  discoverable  in 
the  tissues  which  our  present  methods  of  pathological  investigation 
give  us  the  right  to  call  disease,  although  our  knowledge  of  the 


THE   DISEASE    OF   AGE.  17 

changes  which  occur  later  makes  it  highly  probable  that  they  had 
started  early  during  the  period  of  decline,  at  first  remaining  indis- 
tinguishable. As  the  description  is  continued  the  word  decay  is  used, 
and  it  is  called  physiological  decay.  In  later  portions  of  his  work 
Humphrey  describes  the  changes  in  the  body  attendant  upon  old  age, 
— the  alterations  in  the  bones,  the  enlargement  of  some  organs,  and 
the  shrinking  of  other  parts.  Although  the  idea  of  a  physiological 
death  would  be  very  fascinating,  with  the  hope  that  the  time  will  come 
when  human  beings  shall  escape  from  the  world  without  having 
to  suffer  the  humiliations  of  sickness  and  the  pains  of  disease,  yet 
such  an  end  seems  hardly  likely,  for  that  which  has  been  described  as 
physiological  decay  is  identical  in  its  pathological  lesions  with  what 
has  been  called  Bright's  disease,  or  fibrosis,  or,  as  I  have  ventured  to 
call  it,  the  disease  of  age. 


CHAPTER    III. 

THE   ORIGIN    OF    DISEASE. 

ONE  of  the  central  ideas  of  all  that  has  heretofore  been  said  is  that 
many  diseases  arise  in  consequence  of  latent  changes  which  occur 
without  producing  external  evidence  of  disturbance,  and  that  there- 
fore it  is  necessary  to  rearrange  to  some  extent  our  views  in  regard 
to  the  origin  of  disease.  This  thought  might  be  made  to  lead  to 
the  discussion  of  almost  any  subject  connected  with  the  causation  of 
disease,  but  the  effort  will  be  made  to  restrict  it  closely  to  the  central 
idea  and  to  matters  nearly  connected. 

A  very  important,  probably  the  most  important,  secondary  con- 
sideration is  the  fact  that  disease  seldom  confines  itself  to  one  organ. 
This  fact  is  not  usually  given  its  just  weight,  and  disease  has  been 
looked  upon  as  due  to  inflammation  or  degeneration  of  one  organ  or 
another,  without  any  consideration  of  changes  in  related  parts  and 
distant  organs.  A  general  survey  of  the  whole  bodily  condition  and 
study  of  the  relations  of  the  various  parts  one  with  another  is  abso- 
lutely essential  to  advance  our  understanding  of  the  origin  of  disease. 
Cancer  and  sarcoma,  which  a  few  years  ago  were  very  generally  con- 
founded, and  which  even  now  are  not  always  easy  to  differentiate,  have 
probably  been  as  much  studied  as  any  pathological  conditions,  and 
up  to  a  certain  point  are  well  understood.  Their  appearances  under 
many  different  circumstances  have  been  carefully  investigated,  and  so 
well  are  they  known  that  it  is  often  possible  even  to  predict  what  will 
be  their  behavior  in  the  future.  When,  however,  we  come  to  discuss 
their  causes,  it  must  be  confessed  that  so  far  as  concerns  final  know- 
ledge we  are  as  yet  in  absolute  ignorance.  The  utmost  that  can  at 
present  be  accomplished  is  to  reason  from  the  facts  already  collected 
in  such  direction  as  they  appear  to  point.  Formerly  few  considered 
malignant  disease  to  be  connected  with  any  extrinsic  cause,  the  gen- 
eral belief  being  that  it  arose  from  disordered  action  of  the  natural 
component  parts  of  the  body.  At  the  present  time,  however,  the 
world  of  medicine  tends  toward  the  theory  that  the  origin  of  most 
disease  is  extrinsic ;  that  there  are  material  germs,  either  animal  or 
vegetable  in  nature,  and  capable  of  growth  and  reproduction,  which 
18 


THE   ORIGIN   OF   DISEASE.  19 

are  the  causes  of  the  great  majority  of  diseases.  Although  no  one 
ventures  to  assert  that  the  causes  of  cancer  and  sarcoma  are  known, 
there  is  often  a  tone  in  medical  writings  which  seems  to  indicate  that 
those  thinking  upon  the  subject  are  convinced  that  there  is  an  ex- 
trinsic cause,  and  that  it  remains  only  to  discover  it.  In  the  mean 
time,  however,  we  continue  in  entire  darkness  in  regard  to  what  the 
cause  may  be.  Probably  the  most  extraordinary  feature  of  malignant 
disease,  second  to  the  fact  of  its  existence,  is  the  tendency  to  the 
production  of  what  have  been  called  secondary  or  metastatic  deposits. 
Although  no  authorities  assert  that  it  is  known  that  malignant  disease 
is  contagious  or  infectious,  yet  it  seems  to  be  almost  universally  ac- 
cepted that  there  is  something  of  the  nature  of  infection  which  is 
operative  in  producing  the  metastases ;  that  what  is  called  the  pri- 
mary growth  in  some  unknown  way  transfers  a  sufficient  amount  of 
the  venom  which  is  assumed  to  exist  to  distant  parts  and  there  re- 
produces itself.  So  far  as  concerns  final  knowledge  of  the  cause  of 
the  metastatic  process,  we  are  no  nearer  to  it  than  to  an  understanding 
of  the  origin  of  cancer  and  sarcoma,  and  the  generally  accepted  as- 
sumption of  the  infectious  origin  of  metastasis  is  only  a  convenient 
explanation  of  what  in  truth  is  as  yet  entirely  beyond  our  compre- 
hension. 

A  parallel  may  profitably  be  drawn  between  the  malignant  diseases 
cancer  and  sarcoma  and  the  fibroid  process.  It  has  been  men- 
tioned in  Chapter  II.  that  fibrosis  is  the  most  striking  and  charac- 
teristic feature  of  age,  and  it  was  hinted  that,  as  a  result  of  disease, 
conditions  and  lesions  almost  identical  with  those  inevitable  in  age 
are  frequently  to  be  found  in  youth,  and  even  in  infancy.  Clinically  it 
is  found  that  when  death  has  occurred  from  chronic  disease  which 
during  life  was  ascertained  to  have  attacked  some  one  organ,  fibrosis 
being  the  principal  or  an  important  lesion,  the  fibroid  process  is 
seldom  confined  to  the  organ  in  which  it  was  known  to  exist.  For 
example,  in  organic  heart  disease  involving  fibrosis  of  the  muscle 
there  may  be  an  entire  absence  of  symptoms  of  disease  of  other 
organs,  and  yet  it  can  be  confidently  predicted  that  similar  changes 
will  be  found  to  exist  elsewhere.  The  same  is  true  of  contracted 
kidney,  which  is  essentially  a  process  of  fibroid  degeneration.  Its 
companion  lesions  have  been  much  studied  and  are  well  known. 
Fibroid  disease  of  the  heart,  lungs,  liver,  and  spleen,  or  of  some  of 
them,  is  an  almost  invariable  accompaniment  of  contracted  kidney. 
The  fibroid  changes  in  other  places  besides  the  kidneys  are  just  as 


20  THE   ORIGIN  OF   DISEASE. 

much  a  part  of  this  form  of  Bright's  disease  as  metastatic  deposits 
are  of  cancer  and  sarcoma,  and  are  of  just  as  frequent  occurrence. 
The  fact  that  fibroid  degeneration,  which  constitutes  the  essential  path- 
ological change  in  many  forms  of  chronic  disease,  is  usually  wide- 
spread is  most  striking  and  important.  This  characteristic  of  fibrosis 
will  be  more  fully  considered  when  the  discussion  and  illustration  of 
the  pathology  of  the  various  organs  are  reached.  Perhaps  enough  has 
now  been  said  to  illustrate  the  parallelism  between  the  malignant  dis- 
eases cancer  and  sarcoma,  and  fibroid  degeneration.  This  parallelism 
consists  in  the  fact  that  in  the  great  majority  of  instances  neither 
malignant  disease  nor  fibroid  degeneration  is  able  to  confine  itself  to 
a  small  district,  but  manifests  a  tendency  to  spread  over  a  large  extent 
of  territory  in  the  organism  in  which  it  has  once  established  itself. 
In  regard  to  malignant  disease  it  is  commonly  believed,  and  often 
assumed  as  established,  that  its  spreading  is  the  result  of  infection,  of 
the  transfer  of  a  venom  from  place  to  place.  On  the  other  hand,  if  it 
were  asserted  that  there  is  anything  infectious  in  the  nature  of  con- 
tracted kidney  or  of  fibroid  degeneration  of  the  heart,  such  an  idea 
would  only  excite  ridicule.  Cancer  is  the  result  of  riotous  growth  of 
epithelium  and  fibrous  tissue ;  in  soft  cancers  the  epithelium  prepon- 
derates, and  in  the  hard  varieties  the  amount  of  fibrous  material  is 
greatest.  The  growth  takes  place  at  the  expense  of  the  natural  ele- 
ments, which  are  compressed  and  pushed  aside  or  destroyed.  Sar- 
coma is  a  similar  process,  but  mesoblastic  tissue  plays  the  part  that  is 
taken  by  epithelium  in  cancer.  Fibrosis  consists  in  an  unnatural  and 
unhealthy  growth  of  fibrous  tissue,  and  it  also  takes  place  at  the 
expense  of  the  natural  constituents,  which  are  thrust  aside  or  de- 
stroyed just  as  in  malignant  disease.  Morbid  fibrosis  is  of  slower 
progress  than  malignant  disease,  and  the  morbid  fibroid  material  is 
prone  to  inflammation.  It  is  to  the  combination  of  latent  fibroid 
growth  with  inflammation,  mingled  in  every  possible  way,  that  is  due 
the  greatest  part  of  the  chronic  disease  of  old  age  and  middle  life,  and 
even  of  the  young  who  are  prematurely  aged.  The  tendency  to  de- 
structive suppuration  is  a  trait  common  both  to  malignant  disease  and 
to  fibroid  degeneration.  Should  it  be  possible  for  any  one  to  suppose, 
after  reading  the  foregoing,  that  it  has  been  my  intention  to  indicate  a 
belief  that  Bright's  disease,  cardiac  fibrosis,  or  other  similar  condition 
can,  under  any  circumstances,  have  an  infectious  element,  my  under- 
lying thoughts  have  not  been  clearly  suggested.  Further,  if  it  has  not 
been  indicated  that  there  is  absolutely  no  existing  evidence  supporting 


THE   ORIGIN   OF   DISEASE.  21 

the  widely  prevalent  belief  that  the  metastasis  of  cancer  and  sarcoma 
is  due  to  a  process  of  infection,  my  expression  has  lacked  clearness. 
To  sum  the  matter  up  briefly,  the  result  of  a  careful  review  of  the  facts 
that  have  been  ascertained  is  to  make  it  patent  that  the  two  malignant 
diseases  and  fibroid  degeneration  present  many  points  of  parallelism, 
especially  the  remarkable  tendency  that  both  exhibit  to  spread.  The 
spreading  of  the  two  seems  so  similar  that  it  is  hard  to  escape  from  the 
conviction  that  the  reason  is  the  same  in  both  instances.  It  may  be 
asserted  without  fear  of  contradiction  that  the  spreading  of  fibroid  de- 
generation has  nothing  of  the  nature  of  an  infection.  If  it  were  con- 
ceded that  malignant  disease  and  fibroid  degeneration  spread  as  they 
do  owing  to  similar  causes,  and  that  the  spreading  of  fibroid  degener- 
ation is  not  the  result  of  infection,  it  would  follow  as  a  necessary  corol- 
lary that  the  metastasis  of  malignant  disease  cannot  be  of  the  nature 
of  an  infection. 

Before  turning  from  the  subject  of  malignant  disease,  it  may  be  well 
to  mention  one  or  two  curious  facts  bearing  upon  what  has  been  said. 
Sarcoma  is  not  rare  in  youth,  while  cancer  is  a  disease  of  middle 
life  and  of  the  aged.  Sarcoma  is  very  like  inflammation,  and  often 
it  is  impossible  to  distinguish  by  the  appearance  alone  a  sarcomatous 
deposit  from  inflamed  or  granulation  tissue.  No  one  who  has  paid 
close  attention  to  the  subject  can  have  failed  to  notice  how  often,  in 
studying  cancerous  tissues  with  the  microscope,  there  are  found  also 
extensive  disease  of  the  blood-vessels  and  general  fibroid  degenera- 
tion. It  may,  of  course,  be  said  that  this  is  only  what  should  be 
expected,  as  cancer  is  a  disease  of  advanced  life,  and  it  has  been  shown 
that  fibroid  change  and  vascular  disease  are  essential  features  of  age. 
The  association,  however,  of  fibrosis  and  arterial  disease  with  cancer 
is  of  such  very  frequent  occurrence  that,  although  it  would  be  easy 
to  dismiss  it  as  only  coincidence,  it  is  impossible  to  avoid  the  thought 
that  the  fibroid  process,  by  its  effect  upon  the  blood-vessels,  and  thus 
upon  the  circulation,  may  have  some  predisposing  or  even  causative 
relation  to  cancer.  A  singular  condition,  and  one  that  supports  the 
belief  that  cancer  is  only  the  result  of  ill-ordered  growth  of  natural 
constituent  parts,  is  that  it  sometimes  happens  that  there  is  found,  in 
persons  who  have  died  of  other  diseases  and  who  are  evidently  not 
cancerous,  a  growth  having  all  the  characteristics  of  malignant  neo- 
plasms. Such  a  growth  is  illustrated  and  described  in  the  chapter  on 
the  kidney  (page  143).  The  clinical  history  and  results  of  the  post- 
mortem examination  in  this  case  forbid  the  belief  that  the  growth 


22  THE   ORIGIN   OF   DISEASE. 

could  have  been  an  ordinary  cancer.  The  microscopical  appearance 
of  small  sarcomatous  growths  is  less  characteristic  than  that  of  can- 
cers ;  the  contrast  between  the  neoplasm  and  the  natural  tissues  some- 
times, and  between  it  and  inflamed  tissues  always,  is  much  less  sharp. 
It  has  happened  to  me  again  and  again  to  find,  in  the  fat  layer  cover- 
ing inflamed  hearts,  and  in  tubercular  lungs,  deposits  of  round  cells 
presenting  all  the  objective  characteristics  of  sarcoma. 

The  disease  molluscum  fibrosum,  in  which  fibrous  tumors,  often 
to  the  number  of  hundreds,  grow  upon  the  surface  of  the  body,  is 
singular  and  impossible  of  explanation.  In  cases  of  this  disease  a 
tumor  grows,  and  afterward  others  show  themselves  and  the  number 
increases  rapidly.  For  two  or  three  years  the  tumors  continue  to 
increase  in  number  and  to  grow  in  size.  After  an  uncertain  time, 
no  new  tumors  appear,  and  the  existing  ones  cease  to  grow  larger. 
Such  is  very  commonly  the  history  of  the  disease.  One  cannot  help 
perceiving  the  similarity  in  many  respects  between  this  disease  and 
cancer.  The  multiplicity  of  growths  in  widely  separated  parts  of  the 
body  is  the  same  in  both,  and  in  molluscum  fibrosum  the  tumors, 
both  in  their  general  characteristics  and  in  their  microscopical  struc- 
ture, are  just  as  much  heterogeneous  products  as  are  those  of  cancer. 
The  strange  attribute  of  cancer  which  is  named  malignancy  consists 
solely  in  the  fact  that,  once  started,  it  inevitably  progresses  and  in- 
creases until  the  life  of  the  individual  ceases.  So  far  as  can  be  seen, 
there  is  nothing  specific  or  extraordinary  in  the  manner  in  which 
cancer  kills.  Growth  goes  on  until  important  surrounding  parts  are 
destroyed,  the  tumors  themselves  suppurate,  or  the  person  dies  of 
exhaustion  consequent  upon  the  drain  caused  by  the  disease.  The 
conditions  in  molluscum  fibrosum  are  in  every  respect  similar,  except 
that  the  heterogeneous  growths  are  confined  to  the  surface  of  the 
body,  and  that,  instead  of  inevitably  increasing,  they  may  cease  to 
progress  and  remain  as  mere  inconvenient  obstructions.  When  cancer 
and  sarcoma  are  divested  of  all  romance  and  considered  solely  in  the 
light  of  facts,  they  do  not  appear  to  be  more  mysterious  than  other 
pathological  processes,  and  they  are  closely  paralleled  in  many  of  their 
most  essential  peculiarities  by  various  diseases,  as  has  been  mentioned. 

Consumption  is  the  scourge  of  the  temperate  climates,  causing  a 
greater  mortality  than  any  other  disease,  and,  as  the  highest  grades 
of  civilization  and  intelligence  have  always  existed  in  the  temperate 
regions,  its  origin  has  been  diligently  sought.  If  the  discussion  could 
be  confined  to  consumption  of  the  lungs,  for  which  phthisis  pulmo- 


THE   ORIGIN   OF   DISEASE.  23 

nalis  is  an  analogous  term,  it  would  be  comparatively  simple ;  but  so 
soon  as  the  word  tuberculosis  is  introduced  the  matter  becomes  very 
complicated.  No  examination  of  the  subject  could  be  adequate  with- 
out a  consideration  of  tuberculosis,  which,  besides  including  almost 
everything  that  can  be  called  pulmonary  consumption,  is  made  to 
cover  many  other  conditions  of  disease  which  at  different  periods  of 
the  history  of  medicine  have  been  variously  classified.  Perhaps  some 
of  the  difficulties  that  have  obstructed  the  progress  of  the  medical 
observers  and  philosophers  of  the  past  may  be  avoided  if  two  impor- 
tant principles  that  have  already  been  mentioned  are  kept  constantly 
in  mind.  These  are,  first,  that  disease  seldom  confines  itself  to  any 
very  restricted  locality,  and,  second,  that  Nature  has  in  disease  followed 
her  usual  rule  and  drawn  no  abrupt  lines,  and  consequently  different 
diseases  merge  into  one  another  so  that  it  is  often  impossible  to  mark 
the  line  of  separation. 

In  cases  of  pulmonary  consumption  it  will  be  found  that  disease  is 
seldom  confined  to  the  lungs,  but  that  other  and  distant  parts  are 
generally  involved.  Consumption  or  tuberculosis  is  often  intimately 
associated  with  conditions  of  disease  that  make  it  impossible  to  de- 
cide whether  all  the  lesions  are  the  widely  spread  results  of  a  single 
process,  or  whether,  on  the  other  hand,  the  effect  has  been  produced 
by  separate  diseases  which  have  at  the  same  time  existed  in  one  body. 
It  is  this  that  has  caused  the  differences  of  opinion  which  have  existed 
in  regard  to  the  unity  or  duality  of  the  origin  of  consumption.  The 
teachings  of  Niemeyer  effected  a  most  important  advance  in  our 
knowledge  of  this  strange  disease,  in  regard  both  to  its  origin  and  to 
the  possibilities  of  treatment.  It  would  be  impossible  to  give  a  more 
comprehensive  exposition  of  his  views,  and  of  antecedent  doctrines 
which  he  sought  to  confute,  than  can  be  obtained  from  his  Lectures.  * 
He  opens  as  follows :  "  There  is  no  subject  in  the  whole  range  of 
pathology  which  more  urgently  requires  a  thorough  reform  than  that 
of  pulmonary  consumption.  In  this  field  pathological  anatomy  is 
much  in  advance  of  clinical  medicine.  The  term  '  pulmonary  tuber- 
culosis' being  still  the  one  most  commonly  used  for  pulmonary  con- 
sumption shows  that  the  majority  of  the  physicians  and  clinical  teachers 
of  the  day  abide  by  Laennec's  doctrine,  and  recognize  but  one  form  of 
pulmonary  phthisis, — namely,  tubercular  phthisis.  The  dangerous 
tenets  of  Laennecs  doctrine,  '  that  pulmonary  phthisis  is  a  constitu- 

*  Qinical  Lectures  on  Pulmonary  Consumption,  by  Felix  von  Niemeyer;  translated  by 
C.  Baeumler,  The  New  Sydenham  Society,  London,  1870. 


24  THE   ORIGIN   OF   DISEASE. 

tional  disease,  that  it  never  can  develop  itself  out  of  acute  or  chronic 
pneumonia,  or  take  its  rise  from  a  bronchial  haemorrhage,  or  from  a 
neglected  or  protracted  cold,'  are  up  to  this  day  taught  in  the  medical 
schools  as  undisputed  truths,  and  have  in  practice  a  most  pernicious 
effect  on  the  prevention  and  treatment  of  phthisis. 

"  Laennec's  dogma,  that  every  form  of  pulmonary  phthisis  is  caused 
by  a  specific  new  growth  (une  espece  particuliere  de  production  acci- 
dentelle),  and  that  the  cavities  in  the  lung  take  their  origin  alone  in 
the  softening  and  the  evacuation  of  this  growth,  was  simply  a  patho- 
logical hypothesis,  which,  by  the  more  recent  researches  in  the  field  of 
pathological  anatomy,  has  been  entirely  refuted." 

This  quotation  indicates  the  opinion  that  consumption  is  not  in  all 
instances  due  to  a  specific  new  growth,  but  may  arise  in  two  different 
ways.  It  must  always  be  kept  in  mind  that  Niemeyer  uses  the  words 
consumption  and  phthisis  as  synonymous  terms  which  describe  the 
lung  disease  which  has  been  so  long  known,  but  restricts  tuberculosis 
to  a  much  narrower  field,  allowing  its  application  only  to  that  form  of 
phthisis  which  includes  the  deposit  in  the  lung  of  the  specific  new 
growth  which  he  calls  miliary  tubercle.  In  this  view  of  the  duality 
of  origin  lies  the  very  pith  of  the  doctrine  of  Niemeyer.  He  proceeds 
to  endeavor  to  show  that  the  two  causes  are  inflammation  of  the 
respiratory  apparatus  and  its  termination  in  cheesy  metamorphosis 
and  destruction  of  the  lung,  and  the  development  of  tubercles,  or,  as 
it  is  more  commonly  called,  tuberculosis.  The  tubercles  are  generally 
spoken  of  as  miliary  tubercles,  and  Niemeyer  did  not  acknowledge  the 
existence  of  any  other  form.  He  is  decided  in  his  expression  of 
opinion  that  the  large  cheesy  masses  in  the  lungs  which  break  down 
and  form  most  of  the  cavities  are  not  tubercular,  but  result  from 
purely  inflammatory  processes.  What  Niemeyer  meant  by  a  miliary 
tubercle  was  not  that  which  is  indicated  by  the  term  at  the  present 
day, — namely,  the  minute  bodies  which  develop  in  the  meninges  of 
the  brain  and  spine,  and  in  the  coverings  of  the  thoracic  and  abdom- 
inal organs  and  in  the  parietal  layers  of  the  pleura  and  of  the  perito- 
neum. It  is  strange  that  although  he  dwells  so  much  upon  the  im- 
portance of  miliary  tubercles  he  nowhere  distinctly  defines  them,  the 
nearest  approach  to  a  description  being  the  statement  that  they  are 
gray  and  transparent.*  Having  endeavored  to  establish  the  duality  of 
origin  of  consumption,  Niemeyer  divides  the  disease  into  three  forms. 
The  first  form  is  that  which  is  "  brought  about  alone  by  pneumonic 

*  Loc.  cit.,p.  2. 


THE   ORIGIN   OF   DISEASE.  25 

processes  and  their  termination."  Under  this  head  he  develops,  with  a 
lucidity  and  logic  that  are  admirable,  the  opinion  which  has  made  him 
famous,  that  consumption  is  more  often  due  to  chronic  catarrhal  pneu- 
monia than  to  any  other  one  cause.  The  second  form  is  that  in  which 
"  tuberculosis  has  associated  itself  with  the  phthisis."  It  is  striking 
that  when  Niemeyer  came  to  make  a  classification  of  the  disease  for 
the  use  of  clinicians  he  found  it  necessary  to  have  the  mixed  form,  the 
simple  establishment  of  the  duality  of  origin  being  insufficient  for  prac- 
tical use.  This  is  only  another  proof  of  the  correctness  of  that  which 
has  already  been  so  often  reiterated,  that  Nature  draws  no  abrupt  lines 
and  that  diseases  shade  into  one  another.  In  connection  with  the 
second  form  of  consumption  Niemeyer  expresses  in  the  most  decided 
manner  the  opinion  that  tubercles  are  generally  a  secondary  product, 
and  that  tuberculosis  is  mostly  secondary  to  the  action  of  cheesy 
morbid  products.  At  the  same  time  he  enunciates  the  dogma  which 
has  been  more  widely  quoted  than  anything  else  from  his  writings, 
that  ""  the  greatest  danger  to  most  phthisical  patients  is  the  develop- 
ment of  tubercles."  The  third  form  is  "  primary  tubercular  phthisis." 
Niemeyer  clearly  declares  his  belief  in  the  existence  of  primary  tu- 
berculosis as  a  specific  new  growth,  and  goes  out  of  his  way  to 
refute  the  views  of  those  who  have  stated  that  the  doctrine  of  miliary 
tuberculosis  is  founded  on  errors.  In  reference  to  tuberculosis  being 
of  specific  nature,  in  discussing  the  treatment,  after  insisting  upon 
the  curability  of  many  cases  of  consumption,  he  adds  the  following : 
"  Against  that  form  of  phthisis  which  consists  in  a  primary  tuber- 
culosis, as  well  as  against  the  tuberculosis  which  has  been  developed 
in  the  course  of  phthisis,  treatment  is  indeed  impotent."  Niemeyer's 
lectures  contain  many  other  observations  of  great  interest  and  value. 
He  doubts  if  tuberculosis  is  inheritable,  but  believes  in  an  "  inherited 
disposition  to  pulmonary  phthisis."  He  notes  the  frequency  of  phthisis 
in  the  emphysematous,  and  that  an  abundant  formation  of  connective 
tissue  takes  place  in  the  lung  in  consumption.  This  latter  is  a  most 
important  fact,  and  must  be  taken  into  consideration  in  any  discussion 
of  the  disease.  Congestion  of  the  lungs,  he  says,  is  caused  by  exces- 
sive exertion  of  the  body,  and  by  direct  irritation  of  the  lungs  and 
bronchi  by  foreign  bodies,  and  such  congestion  may  be  the  cause  of 
phthisis.  Niemeyer  disapproves  of  the  teaching  of  Buhl  that  phthisis 
is  an  infectious  disease  caused  by  the  reception  into  the  blood  of 
the  "  tubercular  poison,"  and  comparable  to  pyaemia,  small-pox,  etc. 
Buhl's  view  he  thinks  is  too  exclusive  and  goes  further  than  is  war- 


26  THE   ORIGIN   OF   DISEASE. 

ranted  by  the  facts.  The  keen  discrimination  and  temperate  wisdom 
of  Niemeyer  enabled  him  to  note  many  important  facts,  but  occa- 
sionally he  is  led  into  positions  that  are  untenable.  He  teaches  that 
haemoptysis  is  a  prolific  cause  of  consumption,  and  says  that  the 
blood  which  is  exuded  into  the  air-sacs  and  bronchioles  and  not 
expectorated  at  the  time  of  the  hemorrhage  causes  pulmonary  irrita- 
tion and  general  febrile  reaction,  and,  later,  phthisis  and  even  tubercu- 
losis. The  opinion  of  those  who  assert  that  haemoptysis  is  due  to 
the  previous  existence  of  latent  tuberculosis  he  declares  to  be  incor- 
rect, and  says  that  the  hemorrhage  is  much  more  frequently  bronchial, 
and  that  in  such  cases  tuberculosis,  if  it  arise  at  all,  is  secondary  to 
the  bleeding. 

The  weakness  of  this  train  of  argument  lies  in  the  fact  that  there 
is  no  explanation  for  the  hemorrhage  other  than  the  bare  statement 
that  it  is  bronchial.  It  is  inconceivable  that  a  bronchial  hemorrhage 
could  occur  in  a  perfectly  healthy  person,  and,  as  those  subject  to 
haemoptysis  in  most  instances  have  some  form  of  consumption  sooner 
or  later,  in  the  absence  of  any  other  explanation  of  the  bleeding  it  is 
almost  necessary  to  attribute  it  to  the  phthisical  process.  It  is  un- 
generous to  underestimate  the  importance  of  the  work  of  our  prede- 
cessors in  the  fields  of  science,  and  every  one  who  considers  the  state 
of  opinion  before  and  after  the  enunciation  of  the  doctrines  of  Nie- 
meyer must  acknowledge  how  great  was  the  value  of  his  contributions 
to  our  understanding  of  consumption.  At  the  same  time,  however, 
that  he  firmly  established  certain  facts,  he  failed  to  prove  other 
things  which  he  deemed  equally  fixed  and  important.  The  weakest 
point  in  his  argument  is  his  failure  to  draw  clearly  the  lines  of  dis- 
tinction between  tubercular  phthisis  and  phthisis  resulting  from  in- 
flammation. He  gives  no  description  which  is  adequate  to  enable 
others  to  recognize  that  which  he  calls  miliary  tubercle  and  says  is  a 
specific  new  growth  and  incurable.  In  failing  to  draw  clearly  this  dis- 
tinction, he  failed  to  prove  the  central  point  toward  which  his  whole 
argument  was  intended  to  lead, — the  duality  of  origin  of  consumption. 

The  history  of  opinion  in  regard  to  the  origin  of  consumption  is 
most  curious,  and  if  we  do  not  look  back  too  far  into  the  past  it 
presents  a  strange  series  of  oscillations.  Laennec,  who  may  be  called 
the  father  of  the  modern  views  of  consumption,  believed  it  to  be 
always  the  result  of  a  Single  cause,  a  specific  new  growth,  and,  there- 
fore, as  incurable  as  cancer. 

Niemeyer  bestowed  close  attention  upon  the  study  of  the  clinical 


THE   ORIGIN   OF   DISEASE.  27 

history  of  phthisis,  and,  noticing  how  often  it  follows  colds  and  acute 
disease  of  the  lungs,  read  pathology  in  the  light  of  these  facts.  His 
conclusion  was  that  there  must  be  a  dual  origin.  His  mind  could  not 
escape  the  conclusion  which  was  forced  upon  it  that  inflammation 
of  the  air-passages  and  lungs  causes  consumption,  nor  could  he  de- 
cide to  cast  aside  the  doctrine,  at  that  time  accepted,  that  tubercle  is  a 
specific  new  growth ;  there  was,  therefore,  no  escape  from  the  belief 
in  two  causes.  The  doctrine  of  Niemeyer  of  the  duality  of  origin  of 
consumption  of  the  lungs  was  not  accepted  without  dispute.  For 
some  time  after  its  announcement  there  were  many  who  refused  to 
accept  it,  but  gradually  it  forced  its  way,  until  finally  it  attained  the 
position  of  an  established  belief.  Next  came  the  discovery  by  Koch 
of  the  bacillus  tuberculosis.  This  was  received  by  the  world  of  medi- 
cine almost  with  acclaim.  There  was  but  little  expression  of  oppo- 
sition, and  what  there  was  was  drowned  by  the  general  approval.  It 
was  soon  considered  as  established  that  all  cases  of  consumption  of 
the  lungs  are  caused  by  the  presence  and  action  of  the  bacillus.  This, 
of  course,  overturned  the  structure  so  carefully  raised  by  Niemeyer. 
It  became  impossible  longer  to  believe  in  the  duality  of  origin,  and 
the  teaching  of  Laennec  that  consumption  is  always  due  to  one  and 
the  same  cause,  a  specific  new  growth,  became  rehabilitated,  but  with 
this  important  difference:  the  source  of  the  new  growth  had  been  dis- 
covered in  the  bacillus  of  Koch.  At  the  present  time  throughout  the 
civilized  world  it  is  generally  accepted  as  true  that  consumption  of 
the  lungs  is  the  result  of  a  specific  new  growth  which  is  caused  by 
the  bacillus  tuberculosis.  On  the  other  hand,  the  inadequacy  of  any 
such  doctrine  to  explain  all  the  phenomena  is  so  certain  that  the  voice 
of  opposition  cannot  be  silenced,  however  popular  may  be  the  theory 
of  an  infectious  cause. 

From  time  to  time  statements  are  made  and  cases  detailed  which 
throw  doubt  upon  the  reasonableness  of  the  belief  that  consumption 
of  the  lungs  can  be  explained  as  always  due  to  the  one  specific  cause, 
the  bacillus.  As  an  instance  in  point  may  be  mentioned  the  lectures 
of  Clark,*  in  which  the  following  statement  is  made :  "  It  has  been 
alleged  by  Koch — and  is  generally  believed  in  London — that  every 
case  of  phthisis,  as  I  have  defined  it,  is  microbic,  is  associated  with 
and  dependent  upon  the  presence  and  the  action  of  tubercle  bacilli. 
For  my  own  part  I  presume  to  deny  the  allegation,  and  to  contend 

*  Lectures  on  Cases  of  Fibroid  Phthisis,  by  Sir  Andrew  Clark.  The  Lancet,  July  2, 
1892,  vol.  ii.  p.  i. 


28  THE   ORIGIN   OF   DISEASE. 

that,  whilst  the  great  majority  of  cases  of  phthisis  are  bacillary,  there 
is  a  considerable  minority  of  cases  which  are  non-bacillary,  in  which 
at  no  period  of  their  history  can  bacilli  be  found.  .  .  .  Some  years 
ago  I  had  in  my  own  wards  three  cases  of  what  I  designated  as  non- 
bacillary  fibroid  phthisis.  I  invited  two  or  three  of  my  more  distin- 
guished contemporaries  to  examine  these  cases,  and  to  demonstrate 
the  existence  of  the  tubercle  bacillus  in  them.  They  failed,  and 
justifying  their  failure  said,  'These  are  quite  exceptional  cases,  and 
do  not  break  down  our  generalization.'  "  Of  course  the  statement  of 
one  man  or  the  citation  of  a  few  cases  cannot  be  considered  to  avail 
much  to  disprove  a  generalization  such  as  that  which  has  been  built 
around  the  bacillus  tuberculosis.  The  quotation  from  the  lecture 
of  Clark,  therefore,  is  given  not  as  proving  the  correctness  of  his 
contention,  but  simply  because  it  is  an  example  from  an  authori- 
tative source  of  what  always  has  been  and  what  still  continues  to 
be  asserted  by  many  reliable  clinicians.  Their  expression  of  view 
is  of  such  weight  that  it  is  impossible  to  escape  the  conviction  that 
there  are  cases  of  consumption,  especially  some  of  those  of  the  more 
chronic  form  and  usually  classed  as  fibroid  phthisis,  that  cannot  pos- 
sibly be  due  either  to  the  bacillus  or  to  any  other  infectious  cause. 
This  being  the  case,  it  is  necessary  to  believe  that  they  arise  from 
some  disordered  action  of  the  bodily  organism  itself,  or,  to  be  more 
precise,  that  they  result  from  inflammatory  action, — inflammation 
being  given  a  broad  definition,  making  it  cover  that  which  occurs 
in  the  tissues  after  a  great  variety  of  forms  of  injury.  So  soon 
as  it  is  conceded  that  consumption  ever  is  due  to  inflammation,  the 
doctrine  of  the  unity  of  origin  which  is  associated  with  the  bacillus 
of  Koch  falls  to  the  ground,  and  we  are  forced  back  upon  the  two 
horns  of  a  dilemma :  we  must  either  return  to  the  teachings  of  Nie- 
meyer  of  a  dual  origin  or  cast  aside  entirely  the  belief  in  the  bacil- 
lus tuberculosis  as  the  cause  of  consumption.  So  far  as  concerns 
human  beings,  there  is  no  existing  evidence,  either  clinical  or  ex- 
perimental, which  can,  when  judicially  examined,  be  considered  to 
show  conclusively  that  consumption  is  infectious.  With  regard  to 
experiments  upon  the  lower  animals,  there  have  always  been  disputes 
among  the  experts  in  that  field  in  regard  to  the  conclusions  to  be 
drawn  from  tubercle  inoculations.  Moreover,  it  is  not  really  known 
how  far  it  is  safe  to  make  deductions  in  regard  to  disease  in  human 
beings  from  results  obtained  from  experiments  upon  the  lower  animals. 
There  cannot  be  any  question  of  the  existence  of  forms  of  consump- 


THE   ORIGIN   OF   DISEASE.  29 

tion  which  arise  from  inflammation,  and,  such  being  the  case,  it  is 
much  easier  and  more  logical  to  look  upon  the  bacillus  as  does 
Sutton,*  who  says,  "  It  was  looking  for  finer  morbid  changes  that 
brought  forth  the  bacillus  investigation  and  revealed  those  feeders 
on  the  dead." 

Before  the  time  of  the  school  of  Laennec  consumption  was  thought 
to  result  from  inflammation,  and  even  he  was  unable  to  escape  the 
effects  of  that  which  he  saw  among  his  patients,  for,  after  positively 
stating  his  belief  that  tuberculosis  always  has  its  origin  in  a  specific 
new  growth  and  is  as  incurable  as  cancer,  he  contradicts  himself  by 
saying  he  has  known  a  few  instances  of  recovery  after  tubercles  had 
softened  and  caused  the  formation  of  cavities. f  Niemeyer  broke  down 
this  theory  of  unity  of  origin,  and  forced  the  acceptance  again  of  the 
fact  that  colds  and  lung  inflammations  do  cause  consumption.  The 
next  swing  of  the  pendulum  resulted  from  Koch's  discovery  of  the 
bacillus,  which  quickly  brought  into  prominence  again  the  belief  in  a 
single  cause.  Although  this  doctrine  appeared  to  offer  a  resting-place 
for  men's  minds,  which  had  been  disturbed  by  the  frequent  changes  of 
opinion  in  regard  to  the  origin  of  consumption,  and  it  was  therefore 
received  with  favor,  the  voices  of  those  who  studied  the  disease  at  the 
bedside  and  in  the  post-mortem  room  were  never  quite  silenced. 
Expressions  of  which  the  quotation  from  Clark  may  be  taken  as  a 
type  continued  from  time  to  time  to  appear,  and  when  weighed  col- 
lectively they  prove  conclusively  the  existence  of  an  inflammatory 
origin  of  consumption.  Since  it  has  been  proved  that  cases  of  con- 
sumption do  result  from  inflammation,  and  since  at  the  same  time  it 
has  not  been  scientifically  demonstrated  that  the  bacillus  tuberculosis 
ever  is  its  cause  in  human  beings,  but  only  that  the  bacillus  is  present 
in  the  altered  tissues  of  persons  suffering  with  the  disease,  it  is  much 
more  logical  to  believe  that  consumption  is  only  the  result  of  ill- 
ordered  growth  and  disintegration  of  the  natural  component  parts  of 
the  organism.  To  this  conclusion  my  mind  has  been  driven,  after  a 
prolonged  and  patient  examination  of  such  evidence  bearing  upon  the 
subject  as  it  has  been  possible  to  obtain. 

Proceeding  upon  the  basis  that  phthisis  is  not  of  specific  origin  or 

*  Lectures  on  Pathology,  by  H.  G.  Sutton,  p.  194. 

|  De  1' Auscultation  Mediate,  par  R.  T.  H.  Laennec,  Paris,  1819,  tome  premier,  p.  60: 
"  un  assez  grand  nombre  de  faits  me  donnent  la  conviction  intime  que,  dans  quelques  cas, 
rares  a  la  verite,  un  malade  peut  guerir  apres  avoir  eu  dans  les  poumons  des  tubercules  qui 
se  sont  ramollis  et  ont  forme  une  cavite  ulcereuse." 


3o  THE    ORIGIN   OF   DISEASE. 

of  infectious  nature,  it  is  necessary  to  recollect  that  it  often  owes  its 
origin  to  external  conditions,  but  that  these  are  quite  different  from 
infection.  The  influence  of  heredity  is  well  explained  by  the  sen- 
tence of  Niemeyer,  already  quoted,  that  tuberculosis  is  not  inherit- 
able, but  that  there  is  an  "  inherited  disposition  to  pulmonary  phthisis." 
This  expresses  in  simple  language  a  truth  well  known  to  experienced 
physicians.  The  disease,  however,  frequently  originates  from  external 
causes,  which  are  much  more  tangible  than  so  subtle  a  thing  as  an 
inherited  trait.  Neglected  colds,  chronic  bronchitis,  inflammation  of 
the  lungs,  and  pleurisy,  often  are  the  causes  to  start  an  attack  of  phthisis 
which  ends  only  with  the  death  of  the  individual.  Diseases  of  the 
class  named  are  caused  by  exposure  to  cold  or  other  hardships,  by 
any  unhealthy  mode  of  living  which  lowers  the  vitality,  by  dissipation, 
and  by  many  other  conditions. 

Thus  it  is  seen  that  consumption  is,  in  its  origin,  different  from 
cancer  in  that  external  conditions  have  a  larger  influence  in  pro- 
ducing it,  but  they  are  alike  in  that  both  arise  without  the  intro- 
duction into  the  organism  of  any  foreign  substance  as  their  primary 
cause. 

Syphilis  is  a  type  of  disease  having  a  very  different  mode  of  origin. 
For  its  production  direct  contact  is  necessary  with  a  material  poison 
which  exists  only  in  some  other  individual  who  is  at  the  time  syphilitic. 
The  poison  is  of  a  nature  that  precludes  its  transmission  through  the 
air,  passing  from  one  individual  to  another  only  by  means  of  physical 
contact,  or  by  inoculation,  which  amounts  to  the  same  thing.  Thus 
the  process  is  simple  and  easy  to  understand,  but  the  disease  pos- 
sesses the  characteristic  that,  once  started,  unlike  most  diseases  of 
specific  origin,  which  usually  have  a  somewhat  definite  duration,  it 
may  run  on  for  years,  producing  a  train  of  symptoms  and  lesions 
which  are  well  known  to  be  syphilitic  and  which  frequently  end  in 
death.  Although  the  more  remote  tertiary  lesions  are  as  much  a 
part  of  syphilis  as  the  primary  manifestations,  the  poison  becomes 
with  the  lapse  of  time  a  less  and  less  prominent  feature,  and  in  the 
later  stages  has  disappeared.  This  statement  is  insusceptible  of  rigid 
proof,  but  there  is  every  reason  to  believe  it  to  be  true  that,  for  in- 
stance, tertiary  syphilis  of  the  nervous  system  cannot  be  directly  trans- 
mitted. Some  of  the  later  lesions  of  syphilis  cannot  be  distinguished 
except  by  the  history  from  non-syphilitic  cases  of  chronic  disease. 
For  instance,  there  is  nothing  in  the  appearances,  either  gross  or  mi- 
croscopical, to  render  it  possible  to  make  a  distinction  between  dis- 


THE   ORIGIN   OF   DISEASE.  31 

ease  of  the  blood-vessels  or  of  the  nervous  system  due  to  syphilis 
and  that  which  sometimes  occurs  in  the  blood-vessels  and  nervous 
system  in  the  non-syphilitic.  One  of  the  most  marked  traits  of 
the  later  stages  of  syphilis  is  its  tendency  to  cause  the  production 
of  morbid  fibrous  tissue.  It  is  unnecessary  to  multiply  examples, 
but  as  an  instance  of  this  may  be  mentioned  the  lesions  of  the  liver 
which  are  ascribed  to  syphilis.  These  consist  of  scars  principally 
composed  of  fibrous  tissue  which  has  grown  in  an  organ  that  under 
natural  conditions  is  almost  wholly  epithelial.  The  tissue  of  the 
nervous  system,  both  the  brain  and  the  spinal  cord,  when  altered  by 
tertiary  syphilis,  becomes  ordinarily  harder  than  is  natural,  and  any 
one  who  has  studied  the  lesions  carefully  with  the  microscope  will 
agree  that,  in  association  with  other  changes,  the  fibrous  elements  have 
greatly  increased. 

Syphilis,  therefore,  is  a  disease  which  in  its  origin  is  the  opposite  of 
cancer  and  consumption,  for  it  can  arise  only  in  consequence  of  the 
introduction  into  the  body  of  a  specific  material  poison  which  there 
is  reason  to  believe  is  of  a  nature  heterogeneous  from  anything  in  the 
healthy  tissues.  It  resembles  cancer  and  consumption  in  that  its  more 
remote  effect  is  a  tendency  to  produce  morbid  fibrous  tissue  and 
many  lesions  that  are  identical  with  those  common  in  various  forms 
of  chronic  disease.  A  striking  peculiarity  is  the  waning  strength  of 
the  poison  and  its  final  disappearance,  although  the  effects  of  the 
disease  may  not  only  continue,  but  may  actually  become  greater,  so 
as  finally  to  cause  death. 

Another  class  of  disease  is  constituted  by  the  ordinary  contagious 
maladies,  the  poisonous  principles  of  which  pass  from  person  to  per- 
son through  the  air,  without  direct  physical  contact.  It  is  not  neces- 
sary to  enumerate  the  diseases  belonging  to  this  class,  the  largest  part 
of  which  is  made  up  of  the  exanthemata,  although  there  are  others — 
as,  for  instance,  whooping-cough  and  mumps — which  are  not  char- 
acterized by  any  eruption  upon  the  skin,  and  yet  as  certainly  belong 
to  the  actively  contagious  diseases  as  do  measles  and  small-pox.  The 
origin  of  diseases  of  this  class  is  entirely  hidden  from  us,  but  their 
manifestations  have  been  studied  so  that  their  usual  behavior  is  well 
known.  Although  men's  minds  lead  them  to  seek  continually  for 
material  poisons  as  the  sources  of  origin,  still  the  search  remains 
unrewarded.  There  is  no  reason  why  the  poisonous  principles  may 
not  be  different  from  anything  as  yet  known,  for  nothing  has  been 
discovered  that  affords  any  satisfactory  indication  in  regard  to  their 


32  THE   ORIGIN  OF   DISEASE. 

nature.  The  actively  contagious  diseases,  although  their  source-  of 
origin  is  still  beyond  comprehension,  constitute  as  distinct  a  class 
as  any  one  of  those  heretofore  mentioned.  At  the  same  time,  con- 
tagious diseases  afford  another  example  of  the  fact  that  nature  draws 
no  abrupt  lines.  There  are  diseases  which  are  so  near  the  border-line 
that  clinicians  continue  to  dispute  whether  they  are  contagious,  and 
these  are  alternately  placed  in  the  contagious  class  or  elsewhere,  ac- 
cording to  the  oscillations  of  individual  opinion. 

The  origin  of  disease  is  from  two  causes,  extrinsic  and  intrinsic. 
There  have  now  been  mentioned  four  great  divisions  of  disease, 
typified  by  cancer,  consumption,  syphilis,  and  the  ordinary  contagious 
diseases,  such  as  measles.  The  first  two  are  of  intrinsic  and  the 
last  two  of  extrinsic  origin.  Cancer  is  of  purely  intrinsic  origin, 
arising  solely  from  derangement  in  the  working  of  the  organism. 
The  number  of  diseases  belonging  to  the  same  class  with  cancer  is 
very  small.  Consumption  is  also  of  intrinsic  origin,  for  it  too  arises 
from  disordered  action  of  the  organism,  inflammation  playing  the 
principal  part  in  its  production.  It  differs  from  cancer  in  that  ex- 
ternal surroundings  have  often  a  large  influence  in  its  causation. 
Exposure,  dissipation,  hardship,  or  an  accidental  cold  is  often  the 
starting-point  of  consumption.  In  some  cases,  however,  in  which 
the  inherited  tendency  to  phthisis  is  very  strong,  it  is  impossible  to 
discover  that  any  external  influence  has  been  at  work.  Such  persons 
seem  born  to  die  of  consumption,  and  no  amount  of  care  in  the  avoid- 
ance of  possible  external  causes  will  prevent  the  growth  in  the  lungs 
of  the  solid  masses,  called  tubercles,  which  become  larger,  and  then 
soften,  causing  death  despite  every  precaution.  Cases  of  phthisis  of 
this  variety  are  very  like  cancer  in  their  mode  of  origin,  as  they  are 
the  result  of  ill-directed  growth  and  destruction  of  natural  tissues  for 
which  no  cause  as  yet  appears.  The  number  of  diseases  that  must 
be  classed  with  consumption  is  immense,  including  almost  all  those 
of  chronic  form  and  all  those  due  to  atmospheric  influences  and  other 
unhealthy  conditions  of  the  surroundings  and  mode  of  living  of  human 
beings.  Syphilis  is  of  purely  extrinsic  origin,  and  its  poison  is  trans- 
mitted by  physical  contact  only,  being  incapable  of  passing  through 
the  air.  It  stands  entirely  by  itself,  there  being  no  other  disease  of 
exactly  similar  nature.  Its  most  striking  peculiarities  are  that  the 
poison  disappears  during  the  later  periods,  and  that  the  lesions  it  pro- 
duces are  in  many  respects  identical  with  those  of  chronic  inflamma- 
tory diseases. 


THE   ORIGIN   OF  DISEASE.  33 

The  contagious  diseases  so  evidently  constitute  a  class  by  them- 
selves that  it  is  unnecessary  to  say  anything  more  to  demonstrate  this 
fact. 

With  some  one  of  the  four  types  named  all  known  diseases  can  be 
classed.  The  condition  is  the  usual  one  in  science :  the  principle  is 
easy  to  recognize,  but  its  application  is  difficult.  The  division  of 
diseases  into  four  classes  is  sufficiently  broad  and  elastic  to  receive 
them  all,  but  it  is  often  difficult,  sometimes  impossible,  to  know  where 
to  place  individual  forms.  In  some  cases  it  cannot  be  decided  whether 
a  particular  disease  is  of  extrinsic  or  of  intrinsic  origin.  Dysentery, 
for  instance,  is  often  epidemic,  and  yet  it  has  never  been  shown  to  be 
truly  contagious,  or  even  that  there  is  any  extrinsic  cause,  and  it 
seems  likely  that  it  is  due  to  climatic  conditions  and  the  general  sur- 
roundings and  food.  The  difficulty,  therefore,  in  classifying  the  dis- 
ease is  that  it  is  not  sufficiently  understood  to  enable  us  to  place  it. 
Is  it  truly  contagious  and  like  measles  and  small-pox,  or  is  it  simply 
the  result  of  inflammatory  destruction  of  the  mucous  membrane  of  the 
intestine,  and  of  like  nature  with  the  phthisis  which  follows  chronic 
catarrhal  pneumonia  as  described  by  Niemeyer?  Typhoid  fever  is  at 
present  generally  regarded  as  a  specific  disease,  and  most  of  those 
even  who  do  not  believe  that  the  germ  which  causes  it  is  yet  known 
are  satisfied  that  there  is  a  single  specific  cause,  and  that  sooner  or 
later  it  must  be  discovered.  It  is  not  many  years  since  Murchison, 
after  studying  and  tabulating  several  thousand  cases,  expressed  the 
opinion  that  typhoid  (enteric)  fever  may  arise  de  novo  under  circum- 
stances where  the  conditions  necessary  to  its  production  exist.  Since 
this  conclusion  was  enunciated,  absolutely  nothing  has  been  discov- 
ered in  regard  to  the  origin  of  typhoid  fever  which  a  logically  scien- 
tific mind  can  accept  as  proof  that  the  disease  is  specific.  Here  again 
is  met  the  difficulty  of  classification  on  account  of  the  lack  of  under- 
standing of  the  disease.  Diphtheria  is  another  disease  that  has  never 
been  permanently  placed,  because  its  mode  of  origin  is  not  known, 
although  most  persons  at  the  present  time  believe  it  to  be  caused  by  a 
bacillus.  Clinical  investigation  shows  that  it  is  in  many  respects  dis- 
similar from  the  actively  contagious  diseases.  Diphtheria,  typhoid 
fever,  and  scarlet  fever  present  a  number  of  points  of  similarity.  They 
are  not  so  contagious  as  some  other  diseases,  and  they  take  possession 
of  a  locality  and  attack  persons  who  live  within  the  infected  region  in 
a  manner  that  has  no  parallel  in  the  behavior  of  the  ordinary  con- 
tagious diseases.  This  subject  has  been  discussed  by  me  in  an  essay 

3 


34 


THE   ORIGIN   OF   DISEASE. 


published  some  years  ago.*  Many  facts  seem  to  indicate  that  dis- 
eases such  as  the  three  named  can,  when  the  conditions  necessary 
to  their  production  are  brought  together,  arise  de  novo ;  that  they  are 
capable  of  something  very  nearly  like  spontaneous  generation,  but 
that,  once  started,  their  existence  may  be  continued  by  contagion.  A 
sufficient  number  of  instances  has  been  brought  forward  to  indicate 
that  classification  of  disease  is  difficult,  because  it  is  as  yet  impossible 
to  have  any  adequate  understanding  of  many  diseases. 

No  question  can  be  of  greater  importance  to  the  practical  physician 
than  that  of  the  origin  of  disease,  for  so  soon  as  the  origin  is  known 
the  most  important  step  toward  conclusive  diagnosis  has  been  taken. 
It  is  generally  easy  to  ascertain  where  the  original  cause  produces  its 
first  effects,  and  thence  to  follow  the  more  remote  results  until,  as  often 
happens,  the  process  becomes  a  very  complicated  one.  The  diagnosis 
being  certain,  a  satisfactory  prognosis  can  generally  be  made,  and  it  is 
seldom  difficult  to  decide  upon  the  proper  course  of  treatment. 

The  class  of  diseases  in  regard  to  which  our  understanding  has 
most  greatly  advanced  in  the  last  century  is  that  which  owes  its  origin 
to  the  passage  of  time  and  to  the  environment  of  man,  these  being 
the  ordinary  inflammatory  and  chronic  diseases.  In  regard  to  cancer 
and  small-pox,  which  represent  two  different  types  of  disease,  nothing 
new  has  been  learned  except  the  little  acquired  by  the  study  of  the 
microscopical  changes  which  occur  in  the  tissues.  Much  the  same 
may  be  said  of  syphilis.  The  inflammatory  and  chronic  diseases  cause 
an  immense  proportion  of  the  total  bulk  of  the  suffering  and  dis- 
ability and  of  the  deaths  of  human  beings.  At  the  present  time 
there  is  a  tendency  to  regard  diseases  as  belonging  to  one  organ  or 
another,  and  for  this  reason  to  take  a  narrow  view.  To  obtain  a  com- 
prehensive grasp  it  is  necessary  to  consider  the  general  bodily  con- 
dition, and  it  is  of  the  highest  importance  to  remember  that  disease 
does  not  usually  confine  itself  to  a  restricted  territory,  and  that  most 
chronic  and  inflammatory  diseases  are  related,  shading  into  one  an- 
other in  a  way  that  is  wonderful.  The  inevitable  changes  effected  by 
the  passage  of  time  must  not  be  overlooked,  nor  the  fact  that  in  man 
a  bodily  condition  very  similar  to  old  age  often  results  from  his  sur- 
roundings and  mode  of  life,  these  being  sometimes  due  to  his  folly  or 
wilfulness,  at  other  times  to  circumstances  beyond  his  control. 

*  The  Contagiousness  of  Scarlet  Fever,  by  Arthur  V.  Meigs,  The  Medical  Record, 
December  n,  1886,  and  The  Transactions  of  the  Philadelphia  County  Medical  Society, 
1886. 


CHAPTER    IV. 

THE   BLOOD-VESSELS. 

THE  foundation  of  medicine  is  anatomy,  and  so  soon  as  one  goes 
beyond  mere  scientific  medicine  in  order  to  apply  pathological  an- 
atomy and  facts  to  the  management  of  disease  it  becomes  evident 
that  pathological  anatomy  is  an  important  integral  part  of  it.  In 
dealing  with  this  part  of  my  subject  it  will  be  best  to  begin  with  a 
description  of  pathological  conditions  that  have  come  under  my  notice. 
The  observations  were  made  in  the  wards  of  a  general  hospital,  in 
which  are  treated  many  cases  of  chronic  disease,  but  it  will  be  neces- 
sary to  include  other  facts  such  as  commonly  come  under  the  notice 
of  a  physician.  As  all  the  tissues  and  organs  of  the  body  depend 
upon  the  blood-supply  not  alone  for  their  healthy  state,  but  even  for 
their  existence,  it  will  be  best  to  begin  with  a  description  of  lesions  of 
the  blood-vessels. 

Arteries. — The  examination  of  a  great  many  arteries  has  convinced 
me  that  if  one  seeks  for  histological  arteries  among  those  taken  from 
diseased  persons,  such  as  ordinarily  come  to  the  post-mortem  table, 
disappointment  will  be  the  result,  for  no  man  dies  in  health,  unless 
killed  by  injury.  In  studying  arteries,  therefore,  as  they  appear  when 
examined  with  the  unaided  eye  and  when  seen  with  the  microscope, 
the  pathologist  is  at  once  confronted  with  the  difficulty  of  deciding 
what  is  normal  and  what  appearances  are  to  be  considered  the  results 
of  disease.  The  appearance  of  the  tissues  at  an  early  embryological 
period  is  different  from  that  immediately  before  birth,  and  a  much 
greater  difference  exists  between  the  tissues  of  an  infant  and  those  of 
an  old  man ;  but  no  distinct  line  can  be  drawn  separating  one  of  these 
periods  from  another,  as  each  shades  gradually  into  the  next  succeed- 
ing one.  Little  knowledge  is  required  to  distinguish  an  embryo  from 
an  octogenarian,  but  no  degree  of  skill  will  enable  an  anatomist  or  a 
microscopist  by  examination  of  the  tissues  to  decide  the  exact  age  of 
the  individual  from  whom  they  were  taken.  Just  as  there  cannot  be 
found  a  dividing  line  separating  youth  from  age,  because  the  trans- 
ition is  gradual,  so  there  is  no  sharp  separation  of  health  from  disease. 
The  microscopical  examination  of  blood-vessels  is  more  satisfactory  in 

35 


36  THE   ORIGIN   OF   DISEASE. 

its  results  than  is  that  of  organs,  because  there  is  no  vessel  in  the 
human  body  so  large  but  that  a  section  of  it  at  any  particular  point 
can  be  cut  and  examined  in  its  entirety,  Thus  disease  is  more 
likely  to  be  discovered,  and  a  much  better  idea  of  the  general  con- 
dition is  obtained  than  can  be  had  of  any  one  of  the  organs,  from 
which,  if  the  gross  evidence  of  disease  be  absent,  it  is  possible  only 
to  select  hap-hazard  a  piece  for  microscopical  examination.  As  not 
infrequently  one  portion  of  an  organ  is  greatly  diseased  while  the 
rest  is  healthy,  it  must  often  happen  that  important  disease  is  over- 
looked. 

Before  proceeding  to  describe  disease  of  arteries,  it  is  necessary  to 
give  some  account  of  their  histological  state,  in  order  to  make  what 
will  be  said  comprehensible.  For  convenience  of  description,*  arteries 
are  ordinarily  divided  into  three  classes, — small,  medium,  and  large. 
The  first  includes  the  terminal  branches,  the  second  all  the  named 
arteries  of  the  body  except  those  like  the  aorta  and  the  pulmonary 
artery,  which  are  recognized  as  belonging  to  the  third  class.  So  far 
as  concerns  the  adventitia  and  muscular  coat  nothing  need  be  said, 
but  the  intima  differs  so  greatly  in  arteries  of  different  size  that  it  is 
necessary  to  have  an  accurate  conception  of  its  ordinary  histological 
conditions  in  order  to  recognize  disease.  In  arteries  of  the  largest  size, 
of  which  the  aorta  is  the  type,  the  intima  is  thick  and  of  complex  struc- 
ture, being  composed,  from  within  outward,  first,  of  a  layer  of  endothe- 
lium;  second,  of  the  subendothelial  tissue,  which  consists  of  fibrous 
tissue,  elastic  net-works,  and  connective-tissue  cells,  and,  third,  of  the 
fenestrated  membrane  of  Henle.  In  medium-sized  arteries  the  intima 
consists  of  endothelium,  the  subendothelial  layer,  which  is  composed 
of  delicate  fibrous  connective  tissue  with  branched  corpuscles,  and  the 
internal  elastic  membrane,  or,  as  it  will  usually  be  called  in  this  work, 
the  plicated  membrane.  The  subendothelial  tissue  which  separates 
the  endothelium  from  the  plicated  membrane  is  absent  in  the  smaller 
arterioles.  In  such  arterioles,  therefore,  the  intima  consists  simply  of 
the  plicated  membrane  and  a  single  layer  of  endothelial  cells.  This 
anatomical  fact  it  is  very  important  to  remember,  for  most  of  the 
arteries  in  the  body  are  of  this  nature.  Such  arteries  are  too  small 
to  be  seen  to  any  advantage  with  the  naked  eye,  and,  as  they  are 
prepared  and  stained  for  examination  with  the  microscope  by  the 
methods  at  present  commonly  used,  the  plicated  membrane  is  very 
prominent  and  constitutes  an  important  landmark  to  separate  the 

*  Normal  Histology,  by  George  A.  Piersol,  M.D.     Philadelphia,  1893. 


THE   BLOOD-VESSELS.  37 

intima  from  the  muscular  coat.  In  arteries  of  this  size,  therefore, 
any  tissue  lying  inside  the  plicated  membrane,  except  the  single  layer 
of  flattened  endothelial  plates,  may  always  be  considered  as  the  result 
of  diseased  growth.  In  terminal  arterioles  of  the  smallest  size,  in 
which  the  muscular  coat  has  been  reduced  to  a  single  layer  of  cir- 
cularly placed  muscle- cells,  the  intima  consists  of  endothelium  alone, 
there  being  no  plicated  membrane. 

The  commonest  disease  of  arteries  is  thickening  of  the  intima.  A 
greater  or  less  departure  from  the  appearances  which  have  been  de- 
scribed as  histological  exists  in  a  majority  of  the  arteries  which  are 
examined  by  pathologists.  Although  from  the  stand-point  of  pure 
anatomy  it  is  correct  to  say  that  every  variation  from  the  histological 
type  is  properly  named  disease,  it  becomes  necessary  for  the  physician 
to  decide  how  great  a  departure  from  the  normal  standard  must  be 
present  to  be  worthy  of  consideration.  It  happens  that  thickening  of 
the  intima  is  usually  irregular  in  its  distribution  (see  Figs.  4,  5,  and  9), 
being  often  much  greater  upon  one  side  of  an  artery  than  upon  the 
other,  or  existing  as  irregular  swellings  variously  placed.  This  ir- 
regular distribution  of  the  thickening  of  the  intima,  together  with  the 
fact  that  in  all  arteries  except  those  in  the  last  stages  of  degeneration 
the  plicated  membrane  is  present  to  indicate  precisely  the  separation 
of  intima  from  muscularis,  enables  the  pathologist  to  recognize  with 
certainty  the  presence  of  disease.  The  great  importance  of  changes 
in  the  intima  will  at  once  be  recognized  when  it  is  remembered  that 
its  increase  in  thickness  can  take  place  only  at  the  expense  of  the 
capacity  of  an  artery  to  carry  blood,  which  is  the  sole  function  of  the 
arteries.  Arteries  answering  exactly  to  the  histological  descriptions 
are  seldom  found  post  mortem,  either  in  private  practice  or  in  hos- 
pitals. The  intima  usually  is  not  a  single  row  of  flattened  endothelial 
cells  placed  within  the  plicated  membrane,  but  is  a  layer  of  connec- 
tive-tissue material  containing  nuclei.  In  old  subjects  and  in  those 
who  have  suffered  long  with  chronic  disease  the  extent  of  this  change 
in  the  arteries  is  commonly  great,  while  in  the  young  and  in  those 
whose  health  has  been  good  there  may  be  little  or  none  of  it.  The 
lesser  grades  of  thickening  of  the  intima  must  therefore  be  looked 
upon  as  necessary  accompaniments  of  advancing  age  in  man,  and  as 
harmless  so  long  as  they  remain  slight.  Their  increase,  however,  is 
dangerous,  for  as  the  intima  grows  in  thickness  the  amount  of  blood 
distributed  to  the  tissue  which  the  artery  supplies  is  inevitably  re- 
duced. The  thickness  of  the  intima  may  be  of  any  conceivable  de- 


38  THE   ORIGIN   OF   DISEASE. 

gree,  from  the  slightest  proliferation  of  the  endothelium  at  one  portion 
of  the  circuit  of  an  artery  (Fig.  8,  c  and  d)  to  total  closure  of  the 
calibre  (Figs.  3  and  13). 

The  muscular  coat,  although  much  less  frequently  diseased  than  the 
intima,  is  also  liable  to  undergo  change;  it  is  often  found  to  be  ir- 
regularly thickened  or  degenerated,  or  even  to  be  both  thickened  and 
degenerated  (Figs.  4,  5,  and  23).  Variation  in  thickness  of  the  mus- 
cularis  around  the  circuit  of  an  artery,  if  of  sufficient  degree  to  attract 
attention,  is  easily  seen,  and  may  always  be  positively  asserted  to  be 
the  result  of  disease,  but  it  is  more  difficult  to  recognize  slight  degrees 
of  degeneration. 

The  fibrous  coat  of  arteries  is,  of  the  three  layers,  the  least  satis- 
factory to  study,  because  it  has  no  definite  external  boundary.  The 
line  of  separation  between  muscularis  and  adventitia  is  easily  deter- 
mined with  the  microscope,  but  to  fix  the  exact  external  boundary  of 
the  latter  is  impossible,  for  the  adventitia  is  continuous  with  the  peri- 
vascular  connective  tissue,  with  which  it  is  identical  in  structure.  It 
would  have  been  better  if  histologists  had  assigned  to  arteries  and 
veins  only  two  coats,  the  intima  and  the  muscularis,  and  had  classified 
what  is  now  named  the  adventitia  or  external  fibrous  coat  as  a  part 
of  the  perivascular  connective  tissue.  The  truth  of  this  observation 
is  demonstrated  by  the  examination  of  any  section  of  tissue  con- 
taining arteries  or  veins,  for  it  is  impossible  to  indicate  a  separation 
between  the  adventitia  and  the  perivascular  connective  tissue.  As 
the  fibrous  coat  itself  has  no  definite  external  boundary,  it  is  evident 
that  the  study  of  its  diseases  is  not  easy,  for  it  is  impossible  to  decide 
whether  changes  outside  the  muscularis  properly  belong  to  the  fibrous 
coat  of  the  artery  or  to  the  perivascular  connective  tissue.  The 
fibrous  coat  is  much  less  frequently  diseased  than  the  muscularis,  and 
still  less  than  the  intima.  If  it  were  acknowledged  that  the  adventitia 
should  not  be  classified  as  a  part  of  the  vascular  system,  but  should  be 
considered  as  belonging  to  the  perivascular  connective  tissue,  and  as 
being  thus  only  a  part  of  the  general  connective-tissue  system,  it 
would  make  an  important  change  in  our  manner  of  looking  at  disease. 
The  whole  of  the  great  structure  that  has  been  built  upon  the  doc- 
trines originally  enunciated  by  Gull  and  Sutton  would  have  to  be 
modified.  Their  view  was  that  what  they  named  arterio-capillary 
fibrosis  had  its  origin  in  the  external  fibrous  coat  of  arteries  and  in 
capillaries.  If  my  view  is  correct,  they  were  in  error  in  supposing 
the  condition  to  be  one  of  truly  vascular  origin.  No  conclusive 


FIG.  i. — OBLITERATIVE  ENDARTERITIS  (MODERATE  THICKENING  OF  INTIMA).    (x  20.) 

From  a  woman  of  forty  years  who  died  of  organic  heart  disease.  The  artery  lies  in  the 
fat  covering  the  heart.  ?,  thickened  intima  ;  /,  the  plicated  membrane  ;  m,  the  muscularis  ; 
a,  the  adventitia ;  x,  the  pericardium  ;  }',  a  nerve  ;  z,  the  fat  which  covers  the  heart.  In 
this  instance  the  fat  is  normal  in  appearance. 

FIG.  2. — OBLITERATIVE  ENDARTERITIS  (GREAT  THICKENING  OF  INTIMA).     (x  60.) 

An  artery  from  the  wall  of  the  Fallopian  tube  removed  by  operation  on  account  of  in- 
flammation, a  is  the  adventitia,  which  runs  off  into  perivascular  connective  tissue  ;  m,  the 
muscularis,  and  i,  the  intima,  which  is  so  greatly  thickened  that  only  a  small  irregular 
calibre  remains.  The  diseased  intima,  which  is  structurally  connective  tissue,  is  strikingly 
different  in  appearance  from  the  muscular  coat.  The  latter  is  of  very  uneven  thickness 
and  shades  into  the  intima.  No  trace  of  the  plicated  membrane  remains. 

FIG.  3. — OBLITERATIVE  ENDARTERITIS  (COMPLETE  CLOSURE  OF  THE  VESSEL),     (x  60.) 

An  arteriole  in  the  fat  covering  the  heart  from  a  man  of  thirty  years  who  died  of  organic 
heart  disease.  There  is  very  little  differentiation  of  coats.  The  muscularis  is  less  closely 
knit  together  than  natural,  and  is  not  easily  definable  from  the  tissue  filling  the  calibre. 
This  is  a  loose-meshed  fibrous  material  containing  a  number  of  small  openings.  These 
openings  are  developing  capillaries  and  cross-sections  of  cells  of  which  the  protoplasm 
failed  to  stain.  The  object  depicted  might  be  thought  not  to  be  a  vessel  at  all,  but  for 
the  fact  that  near  it  in  the  section  there  are  others  of  similar  appearance  in  various  stages 
of  closure. 


THE   BLOOD-VESSELS.  39 

evidence  has  as  yet  been  forthcoming  to  demonstrate  the  real  starting- 
point  of  fibroid  disease. 

Various  forms  of  arterial  disease  are  illustrated  by  Figs.  I  to  17 
inclusive.  Figs.  I,  2,  and  3  show  three  stages  of  obliterative  endar- 
teritis.  Fig.  I  may  be  taken  as  a  type  of  the  commonest  form  of  the 
disease.  The  artery  lies  in  the  fatty  covering  of  the  heart  from  a 
woman  forty  years  old  who  died  of  organic  heart  disease  with  nut- 
meg liver  and  increase  of  fibroid  tissue  in  the  spleen  and  kidneys.  In 
an  artery  of  this  size  it  might  be  expected,  perhaps,  that  there  would 
be  some  subendothelial  tissue  between  the  innermost  layer  of  endo- 
thelial  cells  and  the  plicated  membrane,  but  the  intima  is  unevenly 
thick, — a  condition  under  all  circumstances  unnatural, — and  even  at 
the  point  where  it  is  thinnest  it  is  at  least  four  or  five  times  thicker 
than  natural.  When  examined  with  a  higher  power,  such  tissue  may 
be  at  once  recognized  as  pathological.  The  plicated  membrane  is 
very  distinct,  even  with  the  low  amplification  used  in  making  the 
drawing,  and  it  marks  a  definite  line  of  separation  between  the  intima 
and  the  muscular  coat.  The  muscular  coat  also  is  of  uneven  thick- 
ness, and  such  irregularity,  whether  of  the  intima  or  of  the  muscularis, 
is  always  to  be  considered  an  unnatural  condition.  The  theory  which 
attributes  increase  of  thickness  of  the  muscular  walls  of  an  artery  to 
hypertrophy,  and  assumes  that  the  vessel  thereby  acquires  increased 
strength  and  greater  efficiency  of  function,  has  no  foundation  in  fact. 
Nothing  is  known  from  the  clinical  point  of  view  to  show  that  such 
an  artery  has  greater  muscular  power  than  a  healthy  one  with  walls 
of  natural  thickness,  and  the  theory  rests  solely  upon  the  observation 
of  the  fact  that  the  muscularis  does  increase  in  thickness. 

Careful  study  with  the  microscope  of  such  tissue  has  forced  upon 
me  the  conclusion  that  the  process  is  one  of  degeneration,  instead  of 
being  reparative  and  compensatory.  The  amplification  in  Fig.  I  is 
not  sufficient  to  exhibit  the  histological  composition  of  the  muscular 
tissue,  but  in  Figs.  5  and  23,  as  well  as  in  others  of  the  series  of  illus- 
trations, it  is  plain  that  the  muscular  tissue  is  greatly  degenerated  and 
weakened.  The  fibrous  coat  (Fig.  i)  presents  no  positive  evidence  of 
disease,  although  probably  there  is  slight  inflammatory  infiltration 
in  places.  It  demonstrates,  however,  very  well  the  correctness  of  the 
statement  already  made,  that  there  exists  no  landmark  by  which  to  fix 
the  external  boundary  of  the  adventitia.  Is  all  the  fibrous  material 
between  the  muscularis  and  fat  adventitia,  or  is  part  of  it  perivascular 
connective  tissue  ?  And  where  is  the  line  of  separation  ?  In  Fig.  2 


40  THE   ORIGIN   OF   DISEASE. 

is  exhibited  a  more  advanced  stage  of  obliterative  endarteritis.  The 
artery  is  from  the  wall  of  a  Fallopian  tube  removed  by  operation  on 
account  of  inflammatory  disease.  Cell-proliferation  was  excessive; 
the  calibre  of  the  vessel  is  a  mere  slit,  and  the  intima  is  of  enormous 
thickness.  The  structure  of  the  intima  is  that  of  a  rapidly  growing 
fibrous  connective  tissue,  and  in  this  instance  there  is  not  the  slight- 
est appearance  of  any  vascularity.  The  muscularis  is  of  such  very 
different  texture  from  the  intima  that  it  is  easy  to  recognize  the  sepa- 
ration of  the  one  from  the  other  at  all  parts  of  the  circuit,  although 
there  is  no  trace  of  the  plicated  membrane  remaining.  In  arteries 
diseased  to  the  extent  of  this  one  the  plicated  membrane  has  usually 
disappeared.  The  muscular  coat  is  of  very  irregular  thickness  at 
different  parts  of  the  circuit.  The  adventitia  in  this  case,  as  in  Fig.  I, 
demonstrates  the  impossibility  of  giving  it  any  fixity  of  boundaries, 
there  being  nothing  to  mark  the  separation  of  adventitia  from  peri- 
vascular  connective  tissue.  Entire  closure  of  a  vessel  is  illustrated 
by  Fig.  3.  There  is  in  it  no  distinct  differentiation  of  the  coats.  The 
muscularis  shades  gradually  into  the  intima,  which  has  proliferated  so 
as  entirely  to  close  the  calibre.  Although  there  is  no  central  channel 
for  the  passage  of  blood,  there  are  several  small  spaces  toward  the 
middle  of  the  vessel.  It  is  not  possible  in  every  instance  to  understand 
the  nature  of  these  apparent  openings,  but,  so  far  as  can  at  present 
be  known,  they  are  always  either  swollen  spindle-cells  cut  transversely 
or  capillaries  cut  across.  This  subject  will  be  discussed  in  connection 
with  Fig.  23,  at  page  52.  The  general  appearance -of  the  vessel  (Fig. 
3)  is  that  of  an  irregularly  growing  connective  tissue  which  had  been 
subjected  to  the  influence  of  inflammation.  It  might  be  asserted  that 
the  object  is  not  a  vessel,  and  with  some  show  of  reason,  were  it 
not  that  in  the  section  there  are  others  of  somewhat  similar  appear- 
ance, in  various  stages  of  closure,  which  are  certainly  vessels.  This 
artery  lies  in  the  fat-covering  of  the  heart  of  a  man  thirty  years  old 
who  died  of  organic  heart  disease.  Important  effects  of  obliterative 
endarteritis  are  exhibited  by  Figs.  4  and  5.  These  are  two  sections 
of  the  same  artery  cut  less  than  a  quarter  of  an  inch  apart.  The 
calibre  of  the  vessel  has  been  so  greatly  reduced  by  endarterial 
growth  that  its  capacity  to  carry  blood  is  only  a  small  fraction  of 
what  it  was  in  health,  but  in  addition  the  flow  of  blood  was  made 
more  difficult  by  the  irregular  and  changing  shape  of  the  tube  through 
which  it  passed.  As  has  already  been  stated,  one  of  the  striking 
peculiarities  of  the  thickening  of  the  inner  coat  of  arteries  is  the 


FIG.  4. — OBLITERATIVE  ENDARTERITIS  CAUSING  DISTORTION  OF  THE  CALIBRE  OF  THE 

VESSEL.     (X  14.) 

Artery  from  the  heart  of  a  man  of  thirty-two  years  who  died  of  Bright' s  disease  and 
heart  disease.  The  fibrous  and  muscular  coats  and  their  points  of  separation  are  easily 
distinguished.  The  muscular  coat  is  not  of  uniform  thickness.  The  intima  is  enormously 
thickened,  and  irregularly  so  ;  it  is  eight  times  thicker  on  one  side  than  on  the  other. 
On  the  side  on  which  the  intima  is  least  thickened  the  plicated  membrane  can  be  seen 
forming  a  boundary  between  intima  and  musculans.  Opposite,  where  the  intima  is  thick- 
est, the  plicated  membrane  is  lost.  The  calibre  of  the  vessel  is  irregularly  half-moon- 
shaped  instead  of  circular.  Fig.  5  is  another  view  of  the  same  vessel. 

FIG.  5. — OBLITERATIVE  ENDARTERITIS  CAUSING  DISTORTION  OF  THE  CALIBRE  OF  THE 

VESSEL,     (x  H-) 

Section  of  the  same  artery  as  Fig.  4,  and  cut  less  than  a  quarter  of  an  inch  from  it. 
The  thickening  of  the  intima  is  very  irregular,  and  the  separation  of  intima  from  muscularis 
is  in  places  lost.  The  plicated  membrane  has  completely  disappeared.  The  shape  of  the 
calibre  in  this  view  of  the  vessel  is  very  different  from  its  shape  in  Fig.  4  :  such  sudden 
changes  in  the  form  of  the  column  of  blood  within  a  short  distance  must  interfere  with  the 
freedom  of  the  circulation. 


FK;.  4. 


THE   BLOOD-VESSELS.  41 

irregular  and  uneven  method  of  its  growth.  The  process  of  thicken- 
ing is  not  governed  by  any  known  law,  and  the  masses  it  forms  are 
chaotic  in  their  irregularity  of  distribution.  The  freedom  of  the  cur- 
rent of  blood  through  such  a  vessel  as  represented  by  Figs.  4  and  5 
must  be  interfered  with  in  at  least  two  ways.  It  is  well  known  that  a 
circular  tube  carries  a  column  of  liquid  with  the  least  possible  friction 
and  the  greatest .  rapidity,  but  in  Fig.  4  the  opening  is  irregularly 
half-moon-shaped,  and  in  the  acute  angles  not  only  would  a  fluid 
be  checked  in  its  course,  but  eddies  flowing  backward  would  arise. 
Besides,  the  shape  of  the  opening  in  the  vessel  changes,  for  in  Fig. 
5,  which,  as  has  been  stated,  represents  a  portion  of  the  artery  dis- 
tant less  than  a  quarter  of  an  inch  from  that  represented  by  Fig.  4,  the 
opening  is  nearly  circular.  The  changing  of  the  shape  of  the  column 
of  blood  within  so  short  a  distance  would  necessarily  cause  retardation 
of  the  flow,  as  well  as  eddies.  Besides  the  distortion  and  narrowing  of 
the  calibre  of  the  vessel  caused  almost  entirely  by  the  growth  of  the 
intima,  other  interesting  conditions  of  disease  are  illustrated  by  Figs. 
4  and  5.  In  Fig.  4  the  plicated  membrane  can  be  easily  distinguished 
upon  the  side  of  the  vessel  where  the  intima  is  least  thickened.  In 
the  drawing  this  has  not  been  made  so  distinct  as  it  should  have  been, 
and  it  does  not  show  so  well  as  when  greater  amplification  is  used. 
Upon  the  other  side  of  the  vessel  it  has  been  completely  destroyed, 
and  no  trace  of  it  is  anywhere  to  be  seen  in  Fig.  5.  There  is  great 
degeneration  of  the  tissue  at  the  junction  of  the  intima  and  muscularis 
in  Fig.  5,  and  consequently  the  separation  of  them  is  less  distinct  than 
usual.  In  both  drawings  the  muscularis  is  of  uneven  thickness,  but 
the  evidence  of  its  involvement  by  disease  is  much  more  positive  and 
greater  in  Fig.  5  than  in  Fig.  4.  Consideration  of  the  state  of  the 
adventitia,  as  usual,  yields  no  certain  results. 

A  condition  of  disease  of  great  importance  is  shown  by  Fig.  6, 
which  represents  a  longitudinal  section  of  one  of  the  main  branches 
of  the  renal  artery  at  its  point  of  origin.  It  is  from  a  man  of  fifty- 
eight  years  who  died  of  Bright's  disease,  having  greatly  contracted 
kidneys.  As  usual  in  diseased  arteries,  it  is  the  intima  that  has  suf- 
fered most,  it  being  thickened  into  irregular  lumps  which  project  into 
the  calibre  and  obstruct  it.  Morbid  fibrous  tissue  in  its  growth  fre- 
quently produces  an  effect  like  that  which  results  when  a  woman 
sews  too  rapidly :  the  material  is  puckered.  When  the  intima  be- 
comes fibroid  and  lumpy  near  the  branching  of  an  artery,  the  likeli- 
hood of  puckering  is  much  greater  than  in  any  straight  reach  of  the 


42  THE   ORIGIN   OF   DISEASE. 

tube.  Such  puckering  as  illustrated  by  Fig.  6  is  of  very  common 
occurrence,  and  must  be  much  more  injurious  than  the  same  degree 
of  narrowing  at  any  other  part  of  a  vessel.  The  amount  of  blood  to 
be  distributed  to  the  tissue  supplied  by  such  a  vessel  is  greatly  reduced 
at  the  fountain-head.  When  once  a  column  of  blood  of  a  certain  size 
propelled  by  a  given  force  is  in  motion  within  an  artery,  its  speed  will 
be  increased  when  driven  through  narrow  places,  according  to  well- 
known  laws,  but  the  conditions  are  very  different  when  the  entrance 
to  a  branch  artery  at  its  origin  from  the  parent  stem  is  narrowed.  A 
liquid  will  flow  in  the  direction  of  least  resistance,  and  therefore,  when 
the  blood  in  passing  along  an  artery  reaches  a  branch  narrowed  or 
obstructed  at  the  bifurcation,  it  flows  on  in  the  main  stem,  which  is 
the  direction  of  least  resistance,  sending  but  little  into  the  obstructed 
branch,  and  thus  starving  the  tissue  to  which  it  is  distributed. 

In  studying  disease  of  the  heart  it  would  be  almost  impossible  to 
emphasize  too  greatly  the  importance  of  obstruction  at  the  openings 
of  the  coronary  arteries.  There  is  no  part  of  the  human  body  more 
favorable  to  the  development  of  the  condition,  and  none  in  which  it  is 
of  more  frequent  occurrence.  The  aorta,  the  largest  artery  in  the 
body,  and  having  thick  walls,  is  more  prone  than  any  other  to  undergo 
atheromatous  changes.  The  slightest  thickening  of  its  intima  is  liable 
to  distort  and  narrow  the  entrances  to  the  coronary  arteries,  and 
when  once  they  are  narrowed  the  current  of  blood  must  rush  by  in 
the  great  tube,  leaving  the  heart  itself  to  be  starved.  Fig.  6  demon- 
strates no  gross  changes  of  the  muscularis  or  adventitia. 

Fig.  7  illustrates  an  early  stage  of  endarteritis.  The  artery  is  one 
from  the  anterior  surface  of  the  medulla  oblongata  of  a  man  fifty-seven 
years  old  who  died  of  Bright's  disease.  The  changes  are  confined 
to  the  intima.  The  plicated  membrane  is  many  times  thicker  than 
natural,  being  in  places  equal  to  the  muscularis,  and  it  is  opaque  and 
contains  many  rounded  cells  of  large  size.  Flattened  endothelial 
cells  are  to  be  seen  upon  the  inner  edge.  The  appearances  are  pre- 
cisely similar  to  those  which  are  described  as  taking  place  in  the 
cornea  under  the  influence  of  inflammation,  when  it  loses  its  trans- 
parency and  becomes  opaque  and  cellular.  The  appearance  of  this 
vessel  lends  further  support  to  the  statement  already  made,  that  it 
is  a  false  classification  which  includes  a  fibrous  coat  as  a  part  of  an 
artery.  In  this  instance  there  is  nothing  outside  the  muscular  coat  to 
call  adventitia  except  the  delicate  pia  mater,  which  here  represents 
both  fibrous  coat  and  perivascular  connective  tissue. 


FIG.  6. — AN  ARTERY  NARROWED  AT  ITS  ORIGIN.     (X  6.) 

Branch  of  the  renal  artery  from  a  man  of  fifty-eight  years  who  died  of  Bright' s  disease. 
The  vessel  is  cut  longitudinally ;  from  h  to  h  is  one  wall  of  the  main  trunk  ;  the  arrow 
indicates  the  direction  of  the  blood-current  in  the  branch  ;  n  is  placed  in  the  narrow  open- 
ing of  the  branch,  which  at  f  has  its  full  width  ;  /,  #/,  and  a  are  the  intima,  media,  and 
adventitia  respectively ;  c  denotes  points  at  which  the  intima  is  greatly  thickened. 

FIG.  7. — EARLY  STAGE  OF  ENDARTERITIS.     (x  220.) 

An  arteriole  from  the  anterior  surface  of  the  medulla  oblongata  of  a  man  fifty-seven 
years  old  who  died  of  Bright's  disease.  The  intima  only  is  diseased.  The  whole  of  the 
light-colored  tissue  is  the  plicated  membrane,  which  has  grown  so  that  in  places  it  is  as 
thick  as  the  muscularis,  and  instead  of  being  glassy  it  is  muddy  and  contains  many  cells 
which  are  large  and  of  rounded  form.  Flattened  endothelial  cells  are  still  to  be  seen  upon 
the  inner  edge.  In  a  natural  artery  of  this  size  the  intima  should  consist  of  the  clear, 
glassy,  plicated  membrane  and  a  single  layer  of  endothelial  plates.  The  changes  are 
similar  to  those  occurring  in  the  cornea,  which  becomes  opaque  and  cellular  under  the 
influence  of  inflammation.  The  muscular  coat  presents  no  notable  features,  and  the  ad- 
ventitia consists  only  of  the  fine  fibrous  threads  of  the  pia  mater  in  which  the  artery  lies. 


m  a 


FIG.  7. 


THE   BLOOD-VESSELS.  43 

Figs.  8  and  9  illustrate  two  points  in  connection  with  disease  of 
arteries :  Fig.  8  shows  the  beginning  of  endarteritis,  and  Fig.  9  that 
the  disease  may  exist  fully  developed  at  a  very  early  period  of  life. 
The  artery  Fig.  8  is  from  the  anterior  surface  of  the  heart  of  an  infant 
six  months  old  that  died  of  wasting.  The  fibrous  coat  presents  no 
points  of  interest,  The  muscularis  is  of  slightly  uneven  thickness 
and  its  tissue  is  somewhat  degenerated,  but  this  can  be  satisfactorily 
demonstrated  only  by  examination  under  higher  amplification.  The 
intima  presents  several  histological  conditions ;  at  part  of  the  circuit 
it  is  natural,  and  at  other  parts  the  plicated  membrane  has  begun  to 
lose  its  glassy,  translucent  appearance  through  infiltration  of  cells. 
As  this  opacity  increases,  the  intima  thickens  until  there  is  an  area 
of  considerable  thickening,  which  histologically  is  fibrous  connective 
tissue,  and  in  this  region  the  plicated  membrane  has  disappeared, 
having  been  destroyed  by  the  process  of  disease-growth.  The  illus- 
tration is  especially  instructive  as  it  exhibits  the  mode  of  origin  and 
progress  of  thickening  of  the  intima  as  it  comes  on  in  an  infant  that 
died  of  wasting  or  marasmus, — a  disease  that  produces  effects  similar 
to  those  induced  by  many  of  the  chronic  diseases  of  adults.  Ath- 
eroma  is  but  another  phase  of  the  same  disease,  many  of  the  effects 
of  which  are  produced  only  when  the  slow  processes  are  changed 
for  more  rapid  ones;  but  this  is  fully  discussed  elsewhere  (page  54). 
That  disease  of  arteries  involving  degeneration  of  the  muscularis, 
destruction  of  the  plicated  membrane,  and  great  thickening  of  the 
intima  occurs  in  early  infancy  is  fully  proved  by  Fig.  9.  This  artery 
is  from  the  anterior  surface  of  the  heart  of  an  infant  of  five  months 
that  died  of  wasting,  and  it  shows  the  disease  in  its  full  develop- 
ment. The  intima  is  thickened  around  the  entire  circuit  of  the  ves- 
sel, and  there  are  two  lumps  which  project  into  the  calibre :  in  short, 
the  degenerative  process  is  precisely  like  that  so  common  in  the 
vessels  of  adults  who  have  died  of  chronic  disease.  It  is  strange 
that  disease  of  such  a  nature,  which  seems  properly  to  belong  to  the 
aged,  should  also  exist  in  very  young  infants  who  at  the  same  time 
present  many  of  the  appearances  of  age.  The  caricature  of  age  pre- 
sented by  a  foundling  infant  with  marasmus  forms  a  picture  too  well 
known  to  require  comment  Other  methods  of  progress  and  effects 
of  endarterial  growth  are  shown  by  Figs.  10,  11,  14,  and  15.  Figs. 
10  and  II  are  two  arteries  of  nearly  the  same  size  from  a  case  of 
hydronephrosis,  and  they  present  interesting  points  of  similarity  and 
contrast.  Both  have  enormously  thick  walls  and  reduced  calibres, 


44  THE   ORIGIN   OF   DISEASE. 

but  in  Fig.  10  the  muscularis  has  greatly  increased,  being  at  parts  of 
the  circuit  much  thicker  than  the  intima.  Again,  one-third  of  the 
plicated  membrane  has  been  destroyed,  while  it  is  distinctly  visible 
around  the  other  two-thirds  of  the  vessel.  It  is  split  in  two  at  one 
place  before  it  disappears.  In  Fig.  1 1  the  plicated  membrane  is  dis- 
tinct around  the  entire  artery  and  the  muscularis  is  of  uneven  but 
very  slightly  increased  thickness.  The  greater  portion  of  the  thick 
arterial  wall  is  formed  by  the  intima,  which  has  grown  to  immense 
proportions.  In  neither  artery  does  the  adventitia  present  any  notable 
features.  These  sections  show  well  the  structural  difference  between 
the  diseased  intima,  which  is  a  fibrous  connective  tissue,  and  the  mus- 
cular coat,  also  how  the  plicated  membrane  divides  the  two,  and  when 
any  portion  of  the  plicated  membrane  has  been  destroyed,  as  seen  in 
Fig.  10,  how  the  one  shades  into  the  other.  The  most  important 
lesson  of  all  taught  by  the  study  of  these  two  vessels,  which  are  of 
the  same  size  and  were  close  together,  is  that,  although  they  were 
subjected  to  precisely  the  same  disease-influence,  the  effects  produced 
were  so  different.  The  theory  that  disease  of  arteries  commonly  be- 
gins in  the  adventitia  receives  no  support  from  such  vessels  as  these, 
and,  although  the  muscular  coat  is  very  thick  in  one  of  them,  the  ap- 
pearance of  the  tissue  itself  is  such  as  to  foster  the  belief  that  the 
process  is  one  of  degeneration  rather  than  of  hypertrophy  with  an 
increase  of  functional  power. 

In  Fig.  1 1  the  muscularis  is  not  greatly  thicker  than  natural,  while 
the  increase  of  the  intima  has  been  enormous.  Assuming,  for  the 
sake  of  argument,  that  the  thickened  muscularis  of  Fig.  10  had  added 
strength  corresponding  to  its  increased  bulk,  is  it  conceivable  that  it 
could  better  have  accomplished  the  function  attributed  to  it,  of  con- 
tracting the  calibre,  while  there  lay  such  a  mass  of  inert  material  within 
it  as  is  constituted  by  the  thickened  intima  ?  The  appearances  pre- 
sented by  the  two  sections  go  far  to  disprove  the  theory  which  is  so 
generally  accepted,  that  thickening  of  the  muscularis  which  is  common 
is  a  true  hypertrophy.  It  is  not  an  hypertrophy  so  far  as  concerns  the 
arterioles,  for  the  number  of  them  I  have  examined  is  so  great  as  to 
warrant  me  in  making  the  assertion,  but  large  arteries  sometimes 
present  appearances  which  might  be  thought  to  contradict  it,  although 
further  examination  of  the  subject  will  show  that  this  is  not  the  case. 
By  large  arteries  are  meant  such  as  the  radial,  femoral,  and  renal,  in 
all  of  which  it  is  quite  common  to  find  the  muscular  coat  greatly  in- 
creased in  thickness  and  the  intima  at  the  same  time  little  beyond  its 


FIG.  8. — EARLIEST  STAGE  OF  ENDARTERITIS,  FROM  AN  INFANT,     (x  90.) 

An  artery  from  the  anterior  surface  of  the  heart  from  an  infant  six  months  old  that  died 
of  wasting,  f,  adventitia  running  off  into  perivascular  connective  tissue,  and  m,  muscu- 
laris  ;  a,  endothelium,  and  ^,  the  normal  plicated  membrane,  which  has  been  thrown  into 
folds  by  shrinkage.  It  appears  as  a  translucent,  glassy  membrane,  from  which  the  endo- 
thelium has  been  slightly  separated  in  course  of  preparation.  At  c  is  seen  the  earliest  stage 
of  disease.  The  plicated  membrane  is  infiltrated  with  cells  ;  to  the  right  it  is  distinct, 
and  to  the  left  it  disappears  in  growing  cells.  At  d  the  process  is  further  advanced,  neither 
plicated  membrane  nor  endothelium  being  distinguishable,  their  places  having  been  taken 
by  a  layer  of  cellular  material.  At  e  the  intima  is  quite  thick,  looking  exactly  as  it  so 
commonly  does  in  older  issues,  and  the  muscular  coat  outside  of  it  is  thinner  than  else- 
where, probably  because  the  intima  grew  partly  at  its  expense. 

FIG.  9. — ENDARTERITIS,  FROM  AN  INFANT,     (x  45.) 

An  artery  from  the  anterior  surface  of  the  heart  from  an  infant  five  months  old  that  died 
of  wasting.  f\  adventitia,  and  m,  muscularis  ;  a  and  b  indicate  greatly  thickened  portions 
of  the  intima,  which  is  thickened  around  the  entire  circuit.  At  places  the  plicated  mem- 
brane is  distinguishable,  and  again  it  is  lost ;  in  the  thickening  (l>)  it  has  been  entirely 
destroyed ;  it  extends  into  a  upon  both  sides,  and  is  lost  toward  the  middle. 

FIG.  IO.^OBLITERATIVE  ENDARTERITIS.     (x  55.) 

From  a  case  of  hydronephrosis, — an  artery  from  the  kidney.  The  plicated  membrane 
is  a  translucent,  folded  band,  and  is  seen  around  two-thirds  of  the  circuit.  To  the  left, 
around  the  remaining  third  it  has  been  destroyed,  and  the  muscular  coat  and  intima  blend 
into  each  other  in  such  a  manner  that  there  is  no  sharp  boundary  between  them.  In  this 
region  the  muscular  coat  is  much  thickened  and  the  intima  relatively  less  so,  the  effect 
being  that  the  muscular  layer  comes  nearer  to  the  calibre  of  the  vessel  than  at  other  por- 
tions of  the  circuit  in  which  the  plicated  membrane  still  persists.  The  plicated  membrane, 
if  followed  from  right  to  left  above,  is  seen  to  split  into  two  layers  before  it  disappears. 
There  is  great  thickening  of  all  the  coats  ;  the  muscular  layer  is  irregularly  thickened,  and 
the  thickening  of  the  intima  is  immense,  as  it  constitutes  the  largest  part  of  the  vessel- 
wall  :  it  must  be  remembered  that  in  the  natural  condition  the  intima  of  arteries  of  this 
size  is  only  a  thin  layer  of  endothelial  plates  lying  within  the  plicated  membrane.  (Com- 
pare with  Fig.  ii.) 


Fiy. 


' 


FIG.  ii. — OBLITERATIVE  ENDARTERITIS.     (x  55-) 

From  the  same  section  as  Fig.  10  :  another  artery.  The  calibre  is  greatly  narrowed. 
The  intima  is  enormously  and  irregularly  thick,  while  the  plicated  membrane  is  most  dis- 
tinct around  the  entire  circuit.  The  muscular  coat  cannot  be  said  to  be  thicker  than  nor- 
mal, but  it  is  of  irregular  thickness,  which  is  not  natural.  The  two  pictures  demonstrate 
the  irregular  way  in  which  the  walls  of  arteries  thicken  so  far  as  concerns  the  particular 
coat  which  shall  take  on  increase  :  in  the  one  the  increase  is  almost  entirely  of  the  intima ; 
in  the  other  the  muscular  layer  has  suffered  as  much  as  or  more  than  the  intima. 


Flg.ll 


vr'i 


FIG.  12. — RADIAL  ARTERY  WITH  THICKENED  MUSCULARIS.     (x  22.) 

From  a  man  thirty-one  years  old  who  died  of  Bright' s  disease.  The  intima  is  slightly 
and  irregularly  thickened,  while  the  muscular  coat  is  many  times  thicker  than  normal,  and 
its  tissue  is  degenerated.  This  degeneration  of  the  muscularis  is  evident  even  with  the 
low  amplification  used  in  making  the  drawing,  but  is  much  more  so  when  the  section  is 
seen  more  highly  magnified.  The  tissue  is  loose-meshed  and  open,  instead  of  being  closely 
knit  as  healthy  involuntary  muscle  is.  The  intima  is  but  little  thickened  while  the  muscu- 
laris is  very  much  so, — which  is  an  unusual  form  of  disease  of  arteries.  The  muscularis  is 
many  times  thicker  than  natural,  and  greatly  diseased. 


THE   BLOOD-VESSELS.  45 

natural  size.  This  fact  I  have  adverted  to  in  a  paper  published  in 
1888.* 

The  artery  which  seems  most  prone  to  take  on  disease  in  this  form 
is  the  radial.  Fig.  12  represents  the  radial  artery  of  a  man  thirty-one 
years  of  age  who  died  of  Bright's  disease.  The  intima  is  slightly 
thicker  than  natural,  while  the  muscular  coat  is  greatly  increased. 
The  appearance  does  not  suggest  that  there  is  really  an  increase  of 
the  muscular  tissue,  although  the  condition  is  named  hypertrophy  of 
the  muscularis.  The  muscularis,  on  the  contrary,  has  degenerated 
into  a  loose-meshed  and  open  structure,  which  contrasts  strongly 
with  the  close-knit  texture  of  healthy  involuntary  muscle.  Arteries 
of  large  size  are  not  considered  to  have  much  power  to  dilate  and 
contract.  Who  supposes,  for  instance,  that  the  circulation  is  ever  in- 
fluenced by  contraction  of  the  muscular  coat  of  the  aorta  ?  The  large 
arteries  assist  the  current  by  their  elasticity,  which  forces  the  column 
of  blood  onward  during  the  intervals  between  the  heart's  contractions 
and  helps  to  make  even  the  flow.  Questions  of  great  interest  arise  in 
this  connection  regarding  what  is  commonly  called  the  high-tension 
pulse.  High  pressure  within  the  arterial  system  is  usually  inferred 
from  sphygmographic  tracings  and  from  digital  examination  of  the 
radial  pulse.  In  such  cases  the  arterial  walls  are  usually  diseased, 
and,  because  the  arterial  wall  is  often  diseased,  the  question  should 
always  be  asked,  What  influence  has  the  thickened  arterial  wall  in  the 
production  of  the  high-tension  character  of  the  pulse  ? 

Whatever  degree  of  thickening  may  be  found  in  the  muscularis  of 
large  arteries,  it  is  certain  that  in  the  smaller  arterioles  the  commonest 
condition  of  disease  is  thickening  of  the  intima.  This  occurs  in  all 
degrees,  from  the  very  slightest  increase  to  total  closure  of  the  lumen ; 
and,  although  the  muscularis  is  also  often  involved,  thickening  of  it 
alone  without  disease  of  the  intima  is  of  such  rare  occurrence  that  for 
practical  purposes  it  may  be  said  to  have  no  existence. 

Fig.  13  illustrates  entire  closure  of  an  artery.  It  was  taken  from  a 
negro  man  twenty-nine  years  of  age  who  died  of  aneurism  of  the 
aorta.  The  vessel  lay  above  the  aneurismal  sac,  and  was  sufficiently 
near  to  be  within  the  zone  of  inflammation  induced  by  the  growth ; 
this  accounts  for  its  closure.  An  interesting  feature  is  that  so  great 
an  amount  of  disease  could  occur  and  yet  there  be  no  degeneration 

*  A  Study  of  the  Arteries  and  Veins  in  Bright's  Disease,  by  Arthur  V.  Meigs,  Trans- 
actions of  the  College  of  Physicians  of  Philadelphia,  1 888;  printed  also  in  the  Medical 
Record,  New  York,  1888. 


46  THE   ORIGIN   OF   DISEASE. 

of  the  tissue  of  the  vessel  at  any  part.  The  plug  which  fills  the  lumen 
is  formed  of  a  firm  fibrous  tissue,  and  in  it  are  numerous  rounded  and 
elongated  spaces.  Study  of  these  under  greater  amplification  demon- 
strates that  they  are  well-developed  capillaries,  and  that  the  blood- 
supply  of  the  new-formed  tissue  is  quite  rich.  This  cannot  be  de- 
termined from  the  drawing,  because  it  is  not  sufficiently  enlarged,  but 
the  openings  can  be  seen.  The  plicated  membrane  is  very  distinct, 
and  there  is  a  second  between  the  muscular  coat  and  the  adven- 
titia.  This  outer  plicated  membrane,  although  described  as  sometimes 
present  in  arteries,  is  seldom  so  evident  as  in  this  instance.  It  is 
an  unusual  feature  of  the  artery,  for  it  very  seldom  happens  that  it  is 
distinguishable. 

By  Fig.  14  is  represented  a  peculiar  condition  of  disease.  The 
artery  is  from  the  kidney  of  a  man  of  seventy  who  died  of  chronic 
myelitis  and  who  had  also  contracted  kidneys.  In  the  sections  of  this 
kidney  most  of  the  arteries  are  diseased  in  much  the  same  way  as  the 
one  represented,  and  they  present  great  variations  in  detail.  Disease 
of  the  vessels  is  a  necessary  part  of  contracted  kidney.  The  ordinary 
features  of  disease  presented  by  the  artery  are  thickening  and  de- 
generation of  the  walls  and  reduction  of  the  calibre.  It  is  not  worth 
while  to  dwell  further  upon  the  fact  that  all  forms  of  disease  which 
induce  thickening  of  the  walls  of  an  artery  at  the  same  time  reduce 
its  calibre.  This  artery,  however,  demonstrates  a  condition  which  is 
not  shown  by  any  of  the  other  sections.  The  material  forming  the 
arterial  walls  has  undergone  so  great  a  change  that  it  no  longer 
bears  any  resemblance  to  the  tissues  of  which  healthy  arteries  are 
composed.  All  differentiation  of  coats  has  disappeared,  and  the  ar- 
terial wall  is  formed  entirely  of  a  loose-meshed,  coarse,  and  stringy 
fibrous  material  poor  in  nuclei.  At  one  spot  in  the  thickest  part 
of  the  wall  is  a  small  area  in  which  the  tissue  is  disintegrated  and 
granular ;  this  is  probably  a  minute  atheromatous  abscess.  It  con- 
stitutes a  type  of  an  unusual  form  and  degree  of  degeneration. 

Fig.  17  represents  a  minute  arteriole  from  the  kidney  of  an  old 
negro  woman  who  died  of  general  fibrosis,  involving  the  heart, 
lungs,  liver,  spleen,  and  kidneys.  The  vessel  shows  endarteritis  with 
great  reduction  of  the  lumen,  and  there  is  a  small  vessel  in  its  wall 
which  is  unusual  both  in  situation  and  in  appearance.  The  tissue  of 
the  arteriole  is  so  changed  by  disease  and  degeneration  that  but  little 
trace  of  the  usual  component  parts  of  a  healthy  vessel  can  be  distin- 
guished. The  dark-colored  material  farthest  from  the  centre  is  all 


FIG.  13. — OBLITERATIVE  ENDARTERITIS  (COMPLETE  CLOSURE  OF  THE  VESSEL),    (x  12.) 

From  a  negro  man  of  twenty-nine  years  who  died  of  aneurism  of  the  aorta  :  a  small 
artery  attached  to  the  upper  portion  of  the  aneurism,  a,  adventitia,  running  off  into  peri- 
vascular  connective  tissue  ;  x,  an  external  plicated  membrane  sometimes  seen  in  arteries, 
forming  the  boundary  between  the  adventitia  (a)  and  the  muscular  coat  (m)  ;  /,  the  plicated 
membrane,  within  which  the  intima  (?)  has  grown  so  that  it  entirely  occludes  the  lumen 
of  the  vessel.  This  occluding  intima  is  composed  of  a  well-developed  fibrous  tissue,  and 
contains  numerous  capillaries  which  show  to  some  extent  in  the  drawing  as  small  spaces, 
but  which  can  be  well  seen  only  when  the  preparation  is  examined  with  greater  ampli- 
fication. 

FIG.  14. — OBLITERATIVE  ENDARTERITIS.     (x  120.) 

An  artery  from  the  kidney  of  a  man  of  seventy  years  who  died  of  chronic  myelitis  and 
in  whom  the  kidneys  were  contracted.  The  calibre  of  the  vessel  is  very  small  and  is  ec- 
centrically placed,  and  the  walls  are  exceedingly  thick.  The  appearance  and  structure  of 
the  tissue  are  unusual  and  peculiar ;  it  is  more  nearly  uniform  than  common,  and  resem- 
bles connective  tissue  poor  in  nuclei.  It  seems  as  if  the  muscular  coat  had  grown,  and  in 
growing  changed  so  as  to  lose  all  its  ordinary  characteristics.  There  is  no  trace  of  the 
thickened  intima  which  is  generally  the  most  marked  feature  of  endarteritis  in  small  vessels. 
There  are  a  few  renal  tubules  and  epithelial  cells  included  in  the  picture. 

FIG.  15. — DEVELOPING  BLOOD-VESSELS,     (x  120.) 

From  the  same  case  as  Fig.  13  :  a  section  of  the  wall  of  the  aneurism.  The  drawing 
includes  two  adjacent  vessels,  a,  the  lumen  of  the  upper  one  ;  it  is  eccentrically  placed, 
and  the  opening  is  surrounded  by  misshapen  endothelial  cells  ;  b  is  ill-developed  muscular 
tissue.  The  walls  are  enormously  thick,  the  calibre  is  nearly  closed,  and  most  of  the  tissue 
is  like  loose-meshed,  rapidly  growing  connective  tissue.  The  lower  vessel  has  no  opening. 
c  indicates  a  region  in  which  the  lumen  probably  either  had  been  or  was  to  be  developed. 
There  is  no  appearance  of  differentiation  of  coats,  either  intima  or  muscularis,  the  tissue 
being  composed  of  cellular  material  like  connective  tissue.  The  cells  are  arranged  some- 
what in  whorls.  It  might  be  thought  that  neither  of  these  growths  is  a  vessel,  but  they 
were  surrounded  in  the  section  by  others  whose  appearance  established  the  nature  of  the 
two  depicted. 

FIG.  16. — ARTERIOLE  IN  NEW  GROWTH  IN  THE  COLON,     (x  240.) 

A  small  arteriole  from  the  thickened  mucosa  from  a  man  of  twenty-five  years  who  died 
of  dysentery  caused  by  acute  lead  poisoning.  Structurally  the  vessel  bears  no  resemblance 
to  ordinary  arteries,  veins,  or  capillaries,  the  tissue  looking  like  epithelium.  The  mucous 
coat  of  the  colon  in  the  section  from  which  the  drawing  was  made  is  six  millimetres  thick. 


Fig.  13 


Fig.  15 


»HT  10 
!o  barb  otlw  t 


FIG.  17. — ENDARTERITIS  AND  A  MINUTE  VESSEL  IN  THE  WALL  OF  THE  ARTERIOLE. 

(X    220.) 

From  the  kidney  of  a  negro  woman  about  seventy  years  of  age  who  died  of  fibrosis 
involving  the  heart,  lungs,  liver,  spleen,  and  kidneys.  The  lumen  is  almost  closed  by  a 
cobweb-like  mass  of  tissue,  composed  of  nuclei  and  fibrous  strings,  which  is  attached  to 
or  forms  a  part  of  the  vessel-wall.  The  wall  is  much  thickened,  and  all  distinct  differen- 
tiation of  coats  is  lost,  v  is  a  minute  vessel  in  the  wall. 


THE   BLOOD-VESSELS.  47 

that  remains  of  the  muscularis,  while  the  loose,  stringy,  and  richly 
nucleated  connective-tissue  material  is  the  overgrown  intima.  In  ad- 
dition to  the  more  solid  portion  of  the  intima  adjacent  to  the  remains 
of  the  muscular  coat,  there  has  grown  a  tissue  in  the  centre  which 
almost  closes  the  lumen  and  looks  like  cobweb.  This  central  growth 
may  be  taken  as  typical  of  one  of  the  forms  of  endarterial  growth 
that  is  sometimes  seen  in  diseased  vessels.  The  strings  and  shreds 
which  extend  irregularly  across  the  opening  of  the  vessel  present  a 
strange  appearance.  The  blood-carrying  capacity  of  the  arteriole 
must  have  been  almost  nil.  The  minute  vessel  (v)  in  the  wall  might 
be  thought  to  belong  to  the  vasa  vasorum,  or  to  be  a  branch  caught 
in  the  section  so  close  to  its  point  of  origin  that  it  had  not  yet 
escaped  from  the  envelopment  of  its  parent  stem.  It  is  almost 
certain,  however,  that  it  is  a  product  of  disease-growth,  for  in  the 
natural  condition  a  section  of  the  branching  of  an  arteriole  never 
presents  such  an  appearance ;  and  it  is  still  less  likely  to  belong  to  the 
vasa  vasorum,  because  such  minute  arterioles  do  not  have  nutrient 
vessels  in  their  walls. 

Among  all  the  arteries  which  have  thus  far  been  described  there 
is  not  one  which  shows  disease  of  the  fibrous  coat,  except  thicken- 
ing of  the  vasa  vasorum,  and,  although  in  several  the  muscular  coat 
is  diseased,  in  no  instance  in  which  this  is  the  case  has  the  intima 
remained  normal.  On  the  other  hand,  in  several  there  is  disease  of 
the  intima  without  involvement  of  the  other  two  coats.  Most  of  the 
vessels  depicted  are  from  subjects  who  died  of  different  chronic  dis- 
eases, at  ages  varying  from  a  few  months  to  old  age.  The  illustrations 
may  therefore  be  considered  as  representative  of  the  commonest  forms 
of  disease  of  the  arteries. 

It  will  be  seen  from  what  precedes  that  as  a  result  of  the  common 
processes  of  endarteritis  a  great  amount  of  new  solid  material  is 
added  to  the  organism  in  the  form  of  tissue  which  grows  within  the 
arteries.  New  tissue  is  formed  also  in  other  ways,  as,  for  instance,  in 
the  case  of  obliteration  of  the  pericardial  sac  by  pericarditis.  This 
is  not  effected  by  a  simple  adhesion  of  the  parietal  and  visceral  layers 
of  the  pericardium,  but  a  new  tissue  of  greater  or  less  thickness  is 
formed  between,  and  this  new  material  binds  the  two  layers  together. 
A  precisely  parallel  condition  occurs  in  every  case  of  adhesion  of 
one  organ  to  another  or  to  surrounding  structures :  new  material  is 
formed  between  the  opposing  surfaces.  The  development  of  blood- 
vessels in  the  morbid  tissue  formed  inside  of  arteries  and  in  other 


48  THE   ORIGIN  OF   DISEASE. 

new  tissues  will  be  demonstrated ;  and  it  will  be  shown  that,  under 
the  influence  of  disease,  structures  naturally  avascular  become  vas- 
cular. It  is  well  known  that  the  adventitia  of  arteries  and  of  veins 
is  richly  supplied  with  arterioles  and  capillaries  which  supply  it  with 
nutriment,  and  it  is  equally  well  known  that  these  vessels  do  not  pene- 
trate the  muscularis  or  the  intima.  The  muscular  coat  and  the  intima 
therefore  are  in  the  natural  condition  avascular,  and  as  they  lie  between 
the  stream  of  blood  and  the  richly  vascular  adventitia  they  must  de- 
pend for  their  nutriment  upon  the  soakage  into  them  of  blood  from 
one  or  other  of  these  two  possible  sources  of  supply.  Which  of  the 
two  is  the  main  dependence  is  not  certainly  known,  but  it  is  generally 
supposed  that  the  adventitia,  which  contains  what  are  by  common 
consent  named  the  vasa  vasorum,  is  principally  instrumental  in  fur- 
nishing nourishment  to  all  blood-vessels.  It  might  perhaps  better 
be  said  that  this  is  assumed  to  be  the  case,  for  in  truth  there  has 
been  little  evidence  to  decide  the  question.  The  growth  of  a  great 
amount  of  solid  material  within  an  artery  which  has  been  shown 
to  be  one  of  the  common  results  of  endarteritis  suggests  the  question, 
How  is  this  tissue  supplied  with  blood  ?  Tubercles,  being  without 
blood-supply,  are  said  to  disintegrate  as  soon  as  they  have  grown  too 
large  to  be  any  longer  nourished  by  the  soakage  (osmosis)  of  blood 
into  them.  The  case,  however,  is  different  with  the  new  tissue  in 
the  walls  of  arteries,  for,  even  when  there  is  a  great  amount  of  it,  as 
in  Fig.  2,  there  is  no  necessary  sequence  of  decay.  The  growth  of 
vessels  in  the  new  tissue  of  arteries,  in  the  new  material  formed  by 
pericardial  inflammation,  and  in  other  places  naturally  avascular  is 
shown  by  Figs.  3  and  13  and  15  to  27  inclusive.  It  has  been  said 
(page  41)  that  some  of  the  central  spaces  in  Fig.  3  are  to  be  re- 
garded as  vessels,  and  that  the  openings  visible  in  the  material  fill- 
ing the  lumen  of  the  artery  (Fig.  13,  page  46)  are  easily  recognized 
as  well-developed  capillaries  when  the  section  is  examined  with 
higher  amplification.  Fig.  15  shows  a  pair  of  vessels  in  the  wall  of 
the  sac  of  an  aneurism  of  the  aorta  of  a  negro  man  twenty-nine  years 
of  age.  They  are  from  the  same  case  as  Fig.  13.  Even  if  it  be  con- 
sidered that  the  wall  of  the  aneurism  is  but  an  enlargement  of  a 
natural  tissue,  being  produced  by  the  stretching  of  the  aorta,  it  must 
be  confessed  that  it  is  nearly  the  same  as  an  entirely  new  tissue  in  this 
case,  for  the  aneurism  was  an  enormous  sacculated  one  which  grew 
out  from  the  top  of  the  aorta.  It  might  well  be  thought  that  the 
vessels  (Fig.  15)  were  mere  irregular  cellular  growths,  and  not  arte- 


THE   BLOOD-VESSELS.  49 

rioles,  but  in  the  tissue  in  which  they  lay  they  were  surrounded 
by  vessels  of  somewhat  similar  appearance,  whose  varying  conditions 
establish  positively  the  nature  of  the  two  selected  for  the  drawing. 
The  surrounding  vessels  were  in  various  stages  of  growth,  and  were 
seen  to  have  openings  of  different  sizes,  the  appearances  showing 
plainly  that  all  belonged  to  the  vascular  system  and  were  not  mere  ill- 
ordered  cell-growths.  The  mode  of  growth  is  well  shown :  the  cells 
tend  to  arrange  themselves  in  circles  or  sections  of  circles  which  are 
more  or  less  irregular.  This  tendency  of  cells  to  arrange  themselves 
in  whorls  in  young  and  rapidly  growing  tissues  is  well  known  to  his- 
tologists,  being  a  common  appearance,  for  instance,  in  the  skin  of 
young  organisms.  That  it  frequently  occurs  as  a  result  of  pathologi- 
cal conditions  is  sure,  for  it  is  often  seen  in  diseased  tissue  also,  the 
most  familiar  example  being  the  pearly  bodies  of  skin  cancer. 

In  the  vessels  under  consideration  there  is  no  distinct  differentiation 
of  coats,  although  in  the  upper  one  there  is  material  like  ill-formed 
muscular  tissue,  and  the  minute  opening,  which  is  not  centrally  placed, 
is  surrounded  by  cells  resembling  the  endothelial  lining  of  arterioles 
and  capillaries.  The  main  portion  of  both  vessels  is  composed  of  a 
material  which  bears  not  the  slightest  resemblance  to  the  tissues  of 
which  healthy  blood-vessels  are  composed.  It  seems  in  some  respects 
to  resemble  connective  tissue,  and  again  it  is  not  unlike  ill-developed 
epithelium.  In  the  lower  vessel  there  is  no  lumen,  but  one  group  of 
cells  looks  as  if  it  was  the  one  in  which  the  calibre  ought  to  have  been 
developed,  or  in  which  it  had  previously  existed  and  had  been  closed 
by  disease.  The  picture  presents  a  striking  instance  of  exuberant  and 
distorted  cell-growth.  The  common  appearances  of  the  development 
of  blood-vessels  in  embryos  are  well  known,  having  been  watched  at 
all  possible  stages  in  the  chick,  which  presents  the  best  opportunity 
for  their  study,  as  well  as  in  the  human  and  many  other  embryos. 
The  first  stage  of  vessel-formation  is  the  appearance  of  blood-islands ; 
these  are  spaces  with  walls  composed  of  a  single  layer  of  endothe- 
lium,  containing  embryonic  blood-corpuscles.  These  so-called  blood- 
islands  would  have  been  better  named  blood-ponds.  When  first 
formed  they  are  separate  one  from  another,  but  by  their  increase  in 
length  at  either  end  they  become  joined  to  form  tubes,  which  are  the 
earliest  capillaries.  The  walls  of  such  of  these  tubes  as  are  to  form 
capillaries  never  increase  in  thickness,  but  are  composed  of  endothe- 
lium  alone.  On  the  other  hand,  around  such  of  them  as  are  to  be 
arteries  and  veins  the  muscular  coat  and  the  adventitia  grow.  In  the 

4 


50  THE   ORIGIN   OF   DISEASE. 

natural  condition  all  newly  developed  blood-vessels  have  a  distinct 
lumen,  and  their  walls  are  composed  of  a  single  layer  of  endothelial 
cells ;  the  wall  subsequently  thickens  if  the  vessel  is  to  grow  large  to 
become  an  artery  or  a  vein.  The  growth  represented  by  Fig.  15  pre- 
sents an  interesting  problem,  and  one  difficult,  if  not  impossible,  now 
to  understand.  The  appearances  presented  by  these  vessels  and  by 
some  of  those  next  to  be  described  forbid  the  belief  that  they  had 
at  any  time  large  calibres  and  thin  walls,  as  is  natural.  They  must 
have  been  deformed  from  their  very  origin.  Fig.  13  shows  that,  even 
in  the  adult,  capillaries  develop  to  nourish  any  new  tissue  that  may 
grow  in  consequence  of  disease,  and  that  such  are  in  all  respects  like 
the  normal  capillaries.  (See  description  of  the  plate.)  Subsequent 
illustrations,  described  on  page  53,  show  various  stages  of  the  process 
of  vessel-formation.  Besides  this  capacity  of  the  organism  to  develop 
blood-vessels  to  nourish  additions  of  tissue,  another  curious  process 
of  disease  is  illustrated  by  Fig.  15  and  others  of  the  series  of  draw- 
ings. There  seems  to  be  a  natural  tendency  to  produce  blood-vessels 
in  all  tissues,  diseased  as  well  as  healthy,  but  this  conservative  ten- 
dency is  sometimes  overcome.  Fig.  1 5  shows  in  section  two  cylinders, 
one  of  which  is  quite  solid  and  the  other  has  only  a  small  and  ill- 
developed  opening.  It  seems  as  if  the  formation  of  vessels  had  been 
prevented  by  riotous  growth  of  cells,  which  has  produced  useless  solid 
cords  instead  of  tubes  capable  of  performing  the  natural  function  of 
conducting  blood.  In  the  embryo,  tubes  are  formed,  as,  for  instance, 
the  Miillerian  duct  in  a  part  of  its  length,  as  solid  cords  of  cells  in 
which  the  opening  is  afterward  channelled  out,  but  this  does  not 
occur,  so  far  as  is  known,  in  the  case  of  blood-vessels.  It  seems  un- 
likely, therefore,  that  such  deformed  vessels  as  these  shown  by  Fig.  1 5 
could  later  have  opened  to  become  useful  vascular  channels.  Fig.  16 
illustrates  the  production  of  a  vessel  in  tissue  naturally  avascular  when 
such  tissue  has  greatly  increased  in  bulk  owing  to  the  stimulus  of 
inflammation.  It  is  from  the  mucous  coat  of  the  colon  of  a  man  who 
died  in  the  early  stage  of  malignant  dysentery  induced  by  acute  lead 
poisoning.  The  colon  was  enormously  heavy  and  thickened.  The 
mucous  coat  alone,  after  the  tissue  had  been  shrunk  by  being  kept 
in  alcohol  as  a  preservative,  was  six  millimetres  thick,  whereas  the 
entire  thickness  of  the  healthy  colon  would  not  be  one  millimetre. 
The  man  died  before  sloughing  of  the  mucosa  had  begun ;  whence  the 
great  weight  and  thickness  of  the  intestine.  It  is  hardly  necessary  to 
say  that  in  the  natural  condition  the  mucous  coat  of  the  intestine  has 


FIG.  18. — ADHERENT  PERICARDIUM  AND  COMPLETE  OBLITERATION  OF  THE  PERI- 
CARDIAL  SAC,  AND  NEW  BLOOD-VESSELS.     (X  2O. ) 

Section  of  the  heart  and  its  envelopes,  from  a  child  of  ten  years  who  died  of  heart 
disease.  Above  a  is  loose-meshed  fibrous  tissue  ;  it  lies  upon  the  pleural  side  of  the  peri- 
cardium ;  a  to  b  is  the  parietal  pericardium  ;  c  is  the  visceral  pericardium  ;  b  to  c  is  new- 
formed  tissue  lying  between  the  parietal  and  visceral  layers  of  the  pericardium.  The  new 
material  contains  many  vessels  (z/),  and  these  are  cut  in  all  possible  directions.  Between 
c  and  d  is  fat  which  usually  covers  the  heart.  At  c,  the  surface  of  the  heart,  the  fat  is 
condensed  and  thickened,  the  oil-cells  being  smaller  than  elsewhere  ;  e  indicates  vessels 
in  the  fat.  The  dark  masses  in  the  fat  are  strands  of  muscle.  Below  d  is  muscle,  the 
wall  of  the  ventricle.  See  also  Figs.  19  and  20. 


Kic.  18. 


FIG.  19. — NEW  BLOOD-VESSELS,     (x  105.) 

From  the  same  section  as  Fig.  18  :  a  portion  of  the  new-formed  material  between  the 
two  adherent  layers  of  the  pericardium.  It  is  a  loose-meshed  tissue,  containing  many 
blood-vessels,  which  are  curiously  tortuous,  so  that  they  have  been  cut  in  all  directions. 
The  walls  of  most  of  the  vessels  are  not  very  thick, — a  little  more  so  than  ordinary  capil- 
laries, but  not  so  thick  as  arteries, — and  they  are  without  any  differentiation  of  coats. 
a  and  b  are  thicker- walled  than  the  others,  and  both  are  cut  transversely  at  their  upper 
ends.  At  the  upper  end  of  a  the  opening  is  distinct  and  is  ellipsoidal,  while  in  b  it  is 
shadowy  and  seems  as  if  closed  by  cellular  growth.  These  two  are  represented  more 
highly  magnified  in  Fig.  20. 


FIG.  19. 


a 


FIG.  20. — NEW  BLOOD-VESSELS,     (x  220.) 

x  is  a  more  highly  magnified  view  of  b,  Fig.  19  ;  y  is  the  same  differently  focussed ; 
2  is  a  more  highly  magnified  view  of  a,  Fig.  19  ;  x  was  drawn  with  the  microscope  focussed 
upon  the  more  superficial  part.  The  end  included  between  the  two  diverging  lines  from 
c  is  nearly  circular,  and  within  it  is  a  smaller  and  ill-defined  circle  (</),  which  is  the  calibre 
of  the  blood-vessel  plugged  with  cells.  Below  is  the  rest  of  the  cylinder,  and  as  here 
focussed  to  show  its  surface  it  appears  to  be  composed  of  cells  which  are  like  epithelium. 
The  whole  lies  in  a  lymph-space  across  which  pass  minute  threads  (e)  of  connective  tissue 
which  support  and  hold  it  in  position  ;  y  is  the  same  as  x,  but  with  the  microscope  focussed 
upon  a  deeper  layer.  The  upper  end  is  somewhat  ill  defined,  while  the  lower  appears  as 
a  capillary  with  distinct  endothelial  walls  (_/"),  and  outside  these  walls  upon  either  side  is 
a  thick  layer  of  tissue  containing  cells  like  epithelium.  The  lymph-space  with  connective- 
tissue  threads  running  across  it  is  distinct  in  this  view,  z  is  a  in  Fig.  19,  and  in  many 
respects  it  is  like  x  and  y.  It  is  a  developing  vessel  with  thick  walls  which  contain  epi- 
thelial cells  and  is  hung  by  fine  threads  in  a  lymph-space.  The  upper  end  of  the  capillary 
(g]  is  cut  obliquely,  and  is  therefore  more  elliptical  than  circular.  Below  at  h  the  endo- 
thelial walls  are  seen  where  the  capillary  is  cut  lengthwise. 


THE   BLOOD-VESSELS.  51 

no  blood-vessels  in  it  so  large  as  that  depicted,  although  the  rich 
capillary  supply  of  the  villi  of  the  small  intestine  is  well  known.  This 
vessel,  therefore,  which  is  to  be  classed  as  an  arteriole  rather  than  as  a 
capillary,  was  developed  owing  to  the  conservative  tendency  of  nature 
to  give  a  blood-supply  to  all  tissues  which  attain  any  considerable 
bulk.  The  vessel  is  peculiar  not  alone  in  the  fact  that  it  existed  in  the 
mucosa  of  the  colon,  but  also  in  its  structure  and  appearance.  There 
is  no  sign  of  any  differentiation  into  coats,  although  in  a  natural  arte- 
riole of  such  size  the  three  coats  would  be  easily  distinguished ;  nor 
does  the  tissue  of  which  it  is  composed  bear  the  slightest  resemblance 
to  that  of  which  the  walls  of  healthy  vessels  are  formed.  It  looks 
much  more  like  epithelium. 

Another  phase  of  the  development  of  vessels  is  shown  by  Figs.  18, 
19,  and  20.  Fig.  18  represents  a  section  of  heart,  including  the  two 
layers  of  adherent  pericardium;  these,  with  the  new  tissue  between 
them  and  binding  them  together,  are  easily  distinguished.  Fig.  19 
represents  a  portion  of  the  new  tissue  more  highly  magnified,  and  it 
is  seen  to  be  like  connective  tissue  in  structure  and  to  contain  a  great 
many  blood-vessels.  It  is  all  a  new  development,  the  result  of  peri- 
cardial  inflammation ;  its  blood-vessels,  therefore,  are  also  new.  They 
are  numerous  and  tortuous,  and  many  of  them  have  natural-sized 
calibres.  Some  are  so  large  that  if  they  had  been  natural  vessels  they 
would  have  been  classed  as  arterioles  rather  than  as  capillaries.  Al- 
though they  are  of  such  a  size  as  to  render  it  just  to  look  upon  them 
as  arterioles,  and  their  walls  are  as  thick  as  those  of  healthy  arterioles, 
their  structure  is  very  different.  There  is  nothing  like  the  natural 
differentiation  into  coats,  but  the  walls  are  composed  of  a  somewhat 
ill-defined  fibrous  material.  Among  these  vessels  are  two  (a  and  by 
Fig.  19)  which  are  shown  more  highly  magnified  in  Fig.  20.  Their 
walls  are  very  thick,  and  formed  of  tissue  much  more  like  epithelium 
than  like  that  composing  healthy  vessels.  It  looks  as  if  a  thick  wall 
had  grown  outside  the  endothelium.  In  some  places  the  calibre 
appears  to  be  closed.  Altogether  they  present  a  type  very  aberrant 
from  that  of  healthy  blood-vessels  (see  description  of  figures),  and 
they  are  in  many  respects  like  what  is  shown  by  Fig.  15.  Figs.  18, 
19,  and  20,  therefore,  demonstrate  three  things, — the  presence  of  ves- 
sels in  new  tissue,  that  these  at  the  stage  represented  are  structurally 
different  from  healthy  ones  of  equal  size,  and  that  besides  many 
capable  of  performing  their  functions  there  are  many  which  are  closed. 
Such  closed  vessels  are  probably  the  result  of  excessive  and  dis- 


52  THE   ORIGIN  OF   DISEASE. 

orderly  cell-growth,  a  solid  cylinder  having  been  developed  where  a 
tube  was  needed.  There  is  nothing  which  precludes  the  belief  that 
new  vessels  in  new  tissue — such  as  most  of  those  represented  in  Fig. 
19 — would  in  time  have  developed  three  coats  and  have  become  ex- 
actly like  normal  vessels  of  similar  size  and  character. 

The  appearance  of  a  blood-vessel  developed  in  tissue  naturally 
avascular  is  shown  in  Fig.  21.  It  is  from  the  anterior  flap  of  the 
mitral  valve  of  a  youth  fourteen  years  old  who  died  of  organic  heart 
disease.  The  valve  was  greatly  thickened,  and  contained  many  vessels 
similar  to  the  one  figured.  The  opening  of  the  vessel  is  very  small, 
is  eccentrically  placed,  and  is  bounded  at  a  portion  of  its  circuit  by 
nucleated  cells,  which  somewhat  resemble  those  around  the  calibre 
of  the  vessel  depicted  in  Fig.  15.  There  is  no  differentiation  into 
coats,  as  in  healthy  vessels,  and  the  tissue  is  of  such  unusual  appear- 
ance that  it  is  impossible  to  class  it  with  any  one  of  the  healthy 
tissues ;  it  has  not  the  appearance  of  epithelium,  of  glandular,  mus- 
cular, or  connective  tissue,  nor  of  any  of  the  healthy  portions  of  the 
body:  It  is  a  loose-meshed  material  composed  of  fibrous  threads 
and  cells.  The  cells  have  large  nuclei,  around  which  is  struc- 
tureless material,  and  outside  this  is  a  fine  ring,  which  is  the  ex- 
ternal cell-wall.  Again,  there  are  cells  which  appear  simply  as  rings 
enclosing  structureless  material  (see  description  of  figures).  Fig.  22 
represents  cells  similar  to  those  shown  by  Fig.  21,  but  cut  length- 
wise and  magnified  twice  as  much.  A  portion  of  the  tissue  from 
which  the  section  represented  in  Fig.  21  was  obtained  was  cut  per- 
pendicularly to  the  first  plane  of  section,  and  from  this  came  the  ap- 
pearance represented  in  Fig.  22.  The  heavy  edge  shows  the  outer 
portion  of  a  vessel  (see  description  of  figures),  and  the  rest  is  made 
up  of  spindle-cells,  most  of  which  contain  elongated  nuclei.  It  is  easy 
to  understand  why  the  cells  in  Fig.  2 1  appear  as  they  do.  The  cell- 
body  being  composed  of  structureless  material  which  remained  un- 
stained, it  appears  as  an  empty  circle  if  cut  above  or  below  the  nucleus, 
and  as  a  nucleus  surrounded  by  an  empty  space  with  the  circular  cell- 
wall  around  this  if  the  nucleus  be  included  in  the  section.  Such  pecu- 
liar cells  are  not  rare  in  diseased  tissues,  and  will  be  further  discussed. 

Figs.  23  to  27  inclusive  represent  the  same  arteriole  cut  at  various 
levels ;  they  show  an  unusual  form  of  vascular  disease  and  the  de- 
velopment of  blood-vessels  in  new  morbid  tissue.  The  vessel  is  from 
the  lung  of  a  girl  twelve  years  old  who  died  of  organic  heart  disease. 
The  first  section  cut  was  that  from  which  Fig.  23  was  drawn,  and,  the 


.1     Of    1: 


FIG.  21. — DEVELOPING  BLOOD-VESSEL  IN  A  VALVE  OF  THE  HEART.     (X  300.) 

A  transverse  section  of  a  vessel  of  the  thickened  and  diseased  anterior  leaflet  of  the 
mitral  valve,  from  a  youth  of  fourteen  years  who  died  of  organic  disease  of  the  heart.  The 
lumen  is  very  small,  is  eccentrically  placed,  and  around  it  are  some  nucleated  cells  (see 
Fig.  15).  The  vessel  is  almost  a  solid  cord,  and  consists  of  loose-meshed  tissue  con- 
taining cells  of  peculiar  appearance,  a  is  a  cell  composed  as  follows  :  centrally  a  nucleus, 
around  it  a  space  which  looks  empty,  and  externally  a  distinct  cell-wall.  The  empty  ap- 
pearance is  probably  due  to  rapid  growth  of  the  cell,  or  to  the  protoplasm's  having  absorbed 
liquid,  or  to  its  having  contained  colloid  material  which  would  not  stain.  Most  of  the 
cells  are  of  the  character  of  a  ;  b  is  a  cell  cut  across  above  or  below  the  nucleus,  and  thus 
there  appears  only  the  cell-wall  surrounding  an  empty  space  ;  x  marks  the  boundary  of 
the  vessel,  outside  of  which  is  the  diseased  fibrous  tissue  of  the  mitral  valve.  In  the  same 
section  are  to  be  seen  numerous  other  vessels  of  this  nature  in  various  stages  of  develop- 
ment. 

FIG.  22. — DEVELOPING  BLOOD-VESSEL  IN  A  VALVE  OF  THE  HEART,    (x  500.) 

A  longitudinal  section  of  a  similar  vessel  found  in  the  tissue  from  which  Fig.  21  was 
taken,  more  highly  magnified,  a  is  the  outer  boundary  of  the  vessel  (corresponding  to  x 
in  Fig.  21 ) ;  b  is  a  spindle-shaped  cell  with  an  elongated  nucleus  and  distinct  cell- wall ;  it 
has  the  same  appearance  of  emptiness  as  the  cells  in  Fig.  21. 

FIG.  23. — ENDARTERITIS  WITH  BLOOD-VESSELS  IN  THE  NEW  GROWTH,     (x  300.) 

Section  of  an  artery  from  the  lung  of  a  child  of  twelve  years  who  died  of  heart  disease. 
a  is  the  inner  boundary  of  the  vessel ;  b  is  the  plicated  membrane  ;  c,  an  outer  plicated 
membrane  sometimes  seen  in  arteries.  Between  a  and  b  is  the  new  growth,  which  con- 
sists of  a  loose  cellular  material.  The  cells  are  large,  and  many  of  them  have  large 
nuclei  with  spaces  around  them,  and  outside  the  spaces  distinct  cell-walls.  In  the  new 
growth  also  are  vessels  (v]  ;  these  have  endothelial  walls  containing  flattened  nuclei  and 
present  exactly  the  appearance  of  ordinary  capillaries.  The  plicated  membrane  (b}  at 
parts  of  the  circle  is  indistinct  as  a  result  of  disease.  Between  b  and  c  is  the  muscularis, 
which  in  places  (g)  has  degenerated  so  as  to  be  translucent  and  structureless.  Outside  of 
c,  which  is  distinct  throughout  most  of  the  circuit,  is  the  adventitia  running  off  into  peri- 
vascular  connective  tissue.  The  shreds  lying  loose  within  the  calibre  are  bits  of  tissue 
broken  away  from  the  lining,  and  other  sections  show  them  still  attached  :  they  dangled 
in  the  blood-stream. 


Fig.22 


Fig.21 


oss  X)     . 


Fic.^24. — VASCULARITY  OF  THE  NEW  GROWTH  IN  ENDARTERITIS.    (x  220.) 

This  drawing  and  Figs.  25,  26,  and  27  are  from  a  set  of  serial  sections  of  the  artery 
represented  by  Fig.  23.  A  vessel  (v]  at  </is  breaking  through  the  muscular  coat  (m)  of 
the  artery  to  supply  blood  to  the  new  growth  (t). 

FIG.  25. — VASCULARITY  OF  THE  NEW  GROWTH  IN  ENDARTERITIS.     (x  220.) 

The  section  next  below  that  shown  by  Fig.  24.  The  supply-vessel  (v]  is  here  seen  to 
have  passed  quite  through  the  muscularis  (m)  of  the  artery,  f  is  a  large  blood-cell  lying 
in  the  calibre  of  the  supply- vessel  after  its  passage  into  the  new  tissue  (z).  It  is  important 
to  remember  that  there  is  no  connection  between  the  supply-vessel  (v]  and  the  calibre 
of  the  artery. 


FIG.  24. 


THE   BLOOD-VESSELS.  53 

vessels  in  the  new  tissue  having  been  observed,  a  series  of  sixty-eight 
sections  was  prepared,  to  ascertain  if  anything  could  be  found  tending 
to  prove  more  positively  that  these  vessels  are  capillaries,  as  they 
appear  to  be.  The  results  will  be  most  easily  comprehended  from 
the  figures  and  a  detailed  description.  Fig.  23  is  an  arteriole  in  which 
a  large  amount  of  new  tissue  had  developed  inside  the  plicated  mem- 
brane, which  is  distinctly  visible  as  a  zigzag  line  around  the  greater 
part  of  the  circuit.  This  new  growth,  which  is  of  the  intima,  is  of  such 
extent  that  it  forms  a  layer  of  greater  thickness  than  the  muscularis 
and  the  adventitia  together.  The  diseased  intima,  the  growth  of  which 
has  reduced  the  calibre  of  the  arteriole  to  a  very  small  proportion  of 
what  it  once  was,  is  made  up  of  tissue  resembling  that  shown  in  Fig. 
21,  so  far  as  the  appearance  of  the  cells  is  concerned.  These  have 
large  nuclei  and  distinct  external  cell-walls,  the  protoplasm,  repre- 
sented as  pure  white,  being  structureless  and  unstained.  The  fea- 
ture of  special  interest,  however,  is  the  presence  of  two  blood-vessels 
(Fig.  23,  v)  in  the  overgrown  intima.  Their  walls,  formed  of  thin  en- 
dothelium  in  which  can  be  seen  a  few  flattened  nuclei  (see  description 
of  Fig.  23),  have  the  structure  of  capillaries.  The  plicated  membrane, 
as  already  stated,  is  distinguishable  around  the  greater  part  of  the  cir- 
cuit as  a  somewhat  indistinct,  wavy  line,  and  outside  of  it  is  the 
irregular  and  much  degenerated  muscular  coat.  Between  the  muscu- 
laris and  the  adventitia  is  an  outer  plicated  membrane,  which  is  some- 
times present  (see  Fig.  13).  The  adventitia  does  not  present  any 
points  of  interest.  Figs.  24  and  25  represent  two  adjoining  sections 
from  the  series  of  sixty-eight.  Only  half  of  the  arteriole  is  included 
in  these,  as  they  are  intended  to  demonstrate  the  growth  of  nutrient 
vessels  in  the  new  tissue.  Fig.  24  shows  the  entrance  of  a  vessel  into 
the  thickened,  diseased  intima.  This  vessel  is  to  be  classed  as  a  large 
capillary  or  a  small  arteriole,  and  its  walls  are  similar  in  structure  to 
those  already  described  (see  page  51,  and  Fig.  19)  as  common  to 
newly  developed  vessels.  The  new  vessel,  to  reach  the  diseased 
intima,  passes  directly  through  the  muscular  coat.  It  must  be  spe- 
cially remembered  that  the  passage  of  a  blood-vessel  through  or  even 
into  the  muscular  layer  of  an  artery  never  occurs  in  the  natural  con- 
dition. Fig.  25  is  the  section  cut  directly  beneath  Fig.  24,  and  it 
shows  the  nutrient  vessel  after  it  has  passed  farther  into  the  intima. 
There  is  a  large  cell  lying  in  the  calibre  which  must  be  an  embryonal 
blood-corpuscle,  as  it  is  not  like  anything  belonging  to  the  solid 
tissues.  That  this  vessel  (Figs.  24  and  25,  v)  was  a  nutrient  supply- 


54  THE   ORIGIN   OF   DISEASE. 

vessel,  and  not  merely  a  branch  passing  out  from  the  main  arteriole, 
is  fully  proved  by  Figs.  24  and  25  and  the  sections  which  were  cut 
beneath  them.  In  Fig.  25  the  capillary  is  seen  to  be  opening  into 
the  tissue  forming  the  thickened  intima,  and  in  the  sections  below,  of 
which  it  has  not  been  thought  necessary  to  have  drawings  made,  it  can 
be  seen  to  divide  into  two  branches  which  disappear  in  the  tissue  of 
the  intima.  These  branches  have  thin  walls  of  endothelium,  and  there 
is  not  the  slightest  indication  anywhere  of  a  connection  with  the 
calibre  of  the  main  arteriole  in  whose  walls  the  whole  system  lies. 

The  development  of  blood-vessels  in  the  tissues  of  the  embryo 
has  already  been  adverted  to.  Figs.  26  and  27,  which  are  from  the 
same  series  of  sections  as  the  preceding,  contain  spaces  in  the 
thickened  and  diseased  intima,  which  are  developing  blood-channels 
like  the  blood-islands  which  are  always  to  be  found  at  a  certain 
stage  in  embryos.  In  Fig.  26  is  seen  a  space  (b)  which  contains 
several  cells.  This  is  undoubtedly  a  blood-island  with  embryonic 
corpuscles ;  for  its  appearance  precludes  the  possibility  of  its  being 
a  large  multinucleated  cell,  and  sections  from  above  and  below  it  show 
that  it  is  an  isolated  space,  and  not  a  cross-cut  of  a  capillary.  There 
was  no  continuity  of  a  channel  either  above  or  below  ;  the  space  was 
therefore  isolated, — a  true  blood-island.  In  Fig.  27  is  a  space  con- 
taining a  three-cornered  body  with  minute  threads  attached  to  its  ends 
toward  the  right.  This  answers  exactly  to  the  descriptions  *  of  the 
protoplasmic  processes  from  which  capillaries  are  developed  and  with 
which  the  endothelial  walls  are  continuous.  That  the  spaces  in  Figs. 
26  and  27  are  developing  blood-islands  as  described  does  not  seem 
to  admit  of  doubt,  and  it  is  likely  also  that  the  nutrient  vessel  (Figs. 
24  and  25)  was  still  unconnected  with  the  general  blood-stream,  and 
therefore  was  not  sufficiently  developed  to  contain  circulating  blood, 
for  the  series  of  sections  failed  to  demonstrate  its  connection  with  any 
other  vessels. 

Atheroma  is  a  term  used  to  designate  many  varieties  of  vascular 
disease.  It  has  been  employed  most  frequently  to  describe  two 
common  lesions  of  the  inner  surface  of  arteries,  the  elevated  yellowish 
areas  and  the  ulcers,  these  being  named  respectively  atheromatous 
patches  and  atheromatous  ulcers.  Recent  knowledge  of  the  processes 
of  vascular  disease  has  outstripped  accepted  classifications  and  names, 
and  this  makes  it  difficult  to  discuss  such  disease  except  by  describing 
minutely  any  particular  lesion  which  is  under  discussion  and  thus 

*  Piersol's  Histology,  loc.  cit. 


,«lb> 


FIG.  26. — DEVELOPING  CAPILLARY  IN  NEW  GROWTH  OF  THE  INTIMA  OF  AN  ARTERY. 

(X   220.) 

Section  from  the  same  series  as  the  two  preceding  figures.  &,  a  blood-space  contain- 
ing cells.  This  might  be  taken  to  be  a  multinucleated  cell.  It  answers  the  description 
given  by  embryologists  of  the  blood-islands  of  Pander.  In  the  sections  above  and  below 
this  there  is  no  connection  with  any  channel  to  show  that  b  is  a  cross-section  of  an  ordinary 
blood-vessel. 

FIG.  27. — DEVELOPING  CAPILLARY  IN  NEW  GROWTH  OF  THE  INTIMA  OF  AN  ARTERY. 

(X220.) 

Section  from  the  same  series  as  the  preceding,  b,  a  blood-space  in  which  is  seen  a 
small  triangular  body  that  answers  exactly  to  the  histological  descriptions  of  the  proto- 
plasmic processes  seen  in  the  early  stages  of  the  development  of  capillaries.  One  point 
of  the  triangular  process  appears  to  be  breaking  through  the  muscularis  (m],  as  if  the 
capillary  was  growing  in  that  direction,  while  to  its  two  other  points  are  attached  fine 
threads  which  look  like  the  endothelial  walls  of  a  capillary  ;  /;/,  the  muscular  coat ;  ?',  the 
overgrown  intima  ;  p,  the  plicated  membrane  visible  in  a  part  of  the  circuit  of  the  artery 
and  marking  the  separation  of  the  muscular  coat  (»/)  from  the  diseased  intima  (z). 


FIG.  26. 


Fir..  27. 


FIG.  28.— AN  ATHEROMATOUS  AND  CALCAREOUS  RADIAL  ARTERY.     (X  20.) 

From  a  man  fifty-seven  years  old  who  died  of  Bright' s  disease.  The  vessel  is  degen- 
erated to  such  a  degree  that  none  of  the  ordinary  boundaries  are  distinguishable.  The 
wall  is  composed  of  grumous  and  coarse  fibrous  material,  and  it  contains  a  number  of 
cavities.  Some  of  these  spaces  were  filled  by  chalky  deposit,  which  was  removed  with 
weak  hydrochloric  acid  before  the  section  could  be  cut,  and  others  are  atheromatous 
abscesses.  The  very  dark-colored  areas  represent  structureless  material.  The  distinction 
of  muscularis  from  intima  having  disappeared,  it  is  impossible  to  know  in  which  of  the 
coats  the  disease  originated. 

FIG.  29. — AN  EARLY  STAGE  OF  ARTERIAL  ATHEROMA.     (X  26.) 

An  artery  from  the  anterior  surface  of  the  medulla  oblongata  of  a  man  fifty-seven  years 
old  who  died  of  Bright' s  disease.  The  seeming  great  thickness  of  the  wall  at  the  top  in 
the  picture  is  probably  due  to  twisting  of  the  vessel  so  that  the  section  is  oblique  instead 
of  directly  transverse.  The  three  tunics  are  easily  distinguished,  and  it  is  evident  that 
the  intima  is  a  good  deal  thickened.  The  most  striking  peculiarity,  to  show  which  the 
illustration  was  made,  is  the  degeneration  which  has  taken  place  between  the  intima  and 
the  muscularis.  At  the  junction  of  these  two  coats  are  several  small  cavities  and  irregular 
dark  lines  which  represent  structureless  tissue.  The  situation  of  these  minute  athero- 
matous abscesses  and  structureless  areas  shows  that  in  this  instance  the  whole  of  the 
process  of  degeneration  began  at  the  junction  of  the  intima  with  the  muscularis.  This 
is  the  situation  occupied  by  the  plicated  membrane  in  healthy  vessels. 


FK;.  28. 


r  .l^v-   x^^^-S^<s^ra^e-^'-p~<*^"^ 
W**Sk*^i§^_-:,    ^-eKT 


FIG.  29. 


THE   BLOOD-VESSELS.  55 

avoiding  the  application  to  it  of  the  names  in  common  use  except  in 
their  most  broad  and  general  sense.  One  may  speak  of  an  aneurism, 
for  instance,  without  risk  of  being  misunderstood,  and  the  application 
of  the  term  atheroma  to  such  patches  and  ulcers  as  have  been  men- 
tioned receives  universal  acceptation.  The  difficulty  of  finding  names 
by  which  satisfactorily  to  designate  particular  arterial  lesions  after 
they  have  been  studied  and  their  nature  ascertained  is  plainly  reflected 
in  standard  pathological  text-books.  Ziegler,*  for  instance,  gives  a 
clear  and  practical  description  of  the  pathological  anatomy  of  arte- 
ries, but  after  reading  it  the  impression  is  left  upon  the  mind  that 
the  naming  of  the  different  lesions  is  very  inadequate.  Clinical  and 
pathological  evidence  seems  to  tend  to  show  that  most  of  the  ordi- 
nary lesions  of  vessels  which  vary  so  greatly  in  appearance  are  never- 
theless closely  related,  and  are  often  only  the  varying  results  of  a 
common  underlying  process.  During  life  arterial  disease  is  discov- 
ered more  frequently  in  the  radial  than  in  any  other  artery,  owing  to 
the  common  practice  of  feeling  the  pulse  at  the  wrist.  There  is  no 
evidence  that  the  radial  is  more  prone  to  disease  than  the  other  large 
arteries,  but  it  is  undoubtedly  a  good  vessel  to  study  post  mortem, 
because  it  is  so  often  known  during  life  to  be  diseased.  So  far  as 
concerns  post-mortem  appearances  the  condition  of  the  aorta  is  best 
known,  for  in  making  autopsies  the  heart  is  almost  always  ex- 
amined, and  this  cannot  be  done  without  the  condition  of  the  aorta 
being  forced  upon  the  attention  of  the  pathologist. 

Fig.  28  represents  the  radial  artery  of  a  man  fifty-seven  years  old 
who  died  of  Bright's  disease.  So  much  calcareous  material  had  been 
deposited  in  the  tissue  that  it  was  necessary  to  decalcify  it  with  acid 
before  a  section  could  be  cut.  Within  the  calibre  lies  a  large  amount 
of  clotted  blood.  The  walls  of  the  vessel  are  degenerated  to  such  an 
extent  that  no  differentiation  of  the  layers  is  recognizable  and  the 
tissue  appears  structureless.  There  are  numerous  nearly  empty 
spaces ;  these  are  either  atheromatous  abscesses  or  the  spaces  occu- 
pied by  calcareous  deposit.  The  picture  presents  a  type  of  arterial 
degeneration  in  its  most  extreme  development.  From  such  an  artery 
as  Fig.  28  it  is,  of  course,  impossible  to  determine  in  which  of  the 
coats  the  disease  had  its  origin,  or  which  of  them  grew  to  form  the 
thickened  diseased  wall.  Fig.  29  is  an  artery  from  the  anterior  sur- 
face of  the  medulla  oblongata  of  the  man  from  whom  Fig.  28  was 
obtained.  It  illustrates  two  points, — the  occurrence  of  thickening  of 

*  Lehrbuch  der  pathologischen  Anatomic,  zweiter  Band,  Seite  52.     Jena,  1892. 


56  THE   ORIGIN   OF   DISEASE. 

the  intima  without  involvement  of  the  other  coats,  and  that  the  de- 
generation which  had  begun  originated  at  the  junction  of  the  intima 
and  the  muscularis.  The  greater  thickness  of  the  upper  wall  is  here 
owing  to  obliquity  of  section,  and  not  to  actual  thickness  of  the  wall 
(see  description  of  Fig.  29).  The  demonstration  made  by  Fig.  29  of 
the  seat  of  origin  of  the  degeneration  is  important,  and  it  is  not  very 
common  to  find  an  artery  at  just  the  stage  to  show  it.  The  minute 
open  spaces  depicted  are  atheromatous  abscesses,  and  the  long,  dark- 
colored  lines  represent  material  which  has  become  structureless  from 
degeneration.  Both  the  abscesses  and  the  structureless  tissue  lie  di- 
rectly between  the  intima  and  the  muscularis,  in  the  region  occupied 
by  the  plicated  membrane  in  healthy  vessels.  In  this  vessel  the  pli- 
cated membrane  has  been  completely  destroyed.  Figs.  7,  28,  and  29 
are  all  from  the  same  patient,  and  they  demonstrate,  first  (Fig.  7), 
thickening  of  the  intima  in  its  earliest  stage ;  second  (Fig.  29),  the 

beginning  of  degeneration,  and, 

FIG.  30.  third   (Fig.   28),  arterial   disinte- 

gration  with   calcification   in    its 
greatest  development. 

Figs.  30,  31,  and  32  are  views 
of  two  growths  upon  the  inner 
surface  of  the  aorta  near  the 
heart.  The  case  was  one  of  an 

An  excrescence  upon  the  inner  surface  of  the  aorta, 

from  a  woman  thirty  years  old  who  died  of  Bright's  irregular  form   of  Bright's  disease 

disease;  drawn  of  natural  size.      The  excrescence  has  •  ,1  •    ,  it 

much  the  shape  of  a  vegetable  fungus,  being  composed  "\     *     WOman      thirty     years     old. 

of  an  expanded  top,  to  which  are  attached  fine  threads  Fig.  3O  IS  One  of  the  growths, 
that  floated  in  the  blood-stream.  The  growth  sprang  «  .  T  . 

from  a  pedicle  which  passed  like  a  root  through  the  natural  S1ZC.       It  IS  an 

wall  of  the  aorta,  the  wall  having  been  eaten  away  by  having  much  the  shape  of  a 
ulceration  to  allow  the  passage  of  the  pedicle.     This  it.  It       •    •          r  1.1 

growth   appeared   to  be   of  similar  nature  with   that  StOOl,  the  Stalk   HSing  IrOm  a  hole 

represented  in  section  and  enlarged  in  Fig.  31.  It  Qr  depression  in  the  aorta.  Fig. 
differs,  however,  in  that  the  opening  through  the  aortic 

wall  is  smaller  and  the  excrescence  larger.  3!    represents    d.    SCCtlOn    through 

the  other  growth,  and  it  shows 

that  there  was  less  projection  into  the  calibre  of  the  aorta,  but  that 
the  intima  and  the  muscularis  were  ulcerated  completely  through, 
allowing  the  blood  to  burrow  into  the  adventitia  so  as  to  form  a 
small  dissecting  aneurism.  The  free  ends  of  the  muscularis  have 
twisted  so  that  they  project  into  the  calibre  of  the  aorta.  There  are 
two  or  three  of  these  projections,  and  each  of  them  is  formed  of  a 
basis  of  muscular  tissue  upon  which  has  been  deposited  a  covering 
of  material  which  examination  under  higher  amplification  shows  to 


FIG.  31. — EARLY  STAGE  OF  AORTIC  ANEURISM,  (x  10.) 

From  a  woman  of  thirty  years  who  died  of  Bright' s  disease.  The  intima  (/)  and 
muscular  coat  (m)  have  been  broken  through  by  the  process  of  disease  and  a  small  dis- 
secting aneurism  formed  whose  wall  is  composed  almost  entirely  of  adventitia  (a).  There 
are  several  cauliflower  excrescences  (^)  which  projected  into  the  calibre  of  the  vessel. 
The  base  or  centre  of  each  of  these  is  a  shred  of  the  muscular  coat,  while  the  outside 
portion  is  clot,  f  is  an  area  represented  in  Fig.  32  more  highly  magnified.  Fig.  30  repre- 
sents another  aneurism  which  was  close  to  the  one  here  depicted. 

FIG.  32. — EARLY  STAGE  OF  AORTIC  ANEURISM.     (X  I05-) 

Enlarged  view  of  the  region  f  in  Fig.  31.  From  a  to  b  is  one  of  the  shreds  of  the 
muscular  coat  (see  description  of  Fig.  31)  forming  the  centre  of  the  excrescence.  The 
drawing  shows  that  at  a  is  a  well-organized  tissue,  while  at  b  it  is  only  clot,  and  that  the 
transition  from  organized  tissue  to  clot  (from  a  to  b)  is  so  gradual  that  it  is  impossible  to 
say  where  the  one  ends  and  the  other  begins.  Everything  included  in  the  drawing  except 
the  band  (a  to  b}  is  clot,  and  it  is  all  ill  defined  except  at  d,  where  it  has  assumed  curious 
forms. 


THE   BLOOD-VESSELS.  57 

be  partly  clot  and  partly  inflammatory  growth.  Fig.  32  represents 
a  portion  of  one  of  the  projections  or  fungous  growths  from  Fig. 
31  (see  descriptions  of  Figs.  30  and  31).  Centrally  from  bottom  to 
top  runs  the  core  which  springs  from  the  muscular  layer.  This  is 
composed  at  the  lower  portion  (Fig.  32,  a)  of  distinct  fibres  inter- 
spersed with  nuclei,  and  is  muscular  tissue  distorted  and  changed  in 
appearance  by  the  ulcerative  process  to  which  it  was  subjected. 
Toward  the  top  the  core  becomes  of  less  and  less  definite  structure, 
until  finally  (Fig.  32,  b]  it  is  simply  clot.  The  material  upon  both 
sides  of  it  is  formed  of  clot,  composed  of  corpuscles  more  or  less 
disintegrated  and  strings  of  fibrin,  and  at  places  this  clot  has  assumed 
curious  circular  forms  (Fig.  32,  </).  Strange  effects  are  often  pro- 
duced in  clots,  caused  by  the  shrinking  that  always  occurs  as  a  result 
of  the  efforts  of  nature  to  remove  them. 

These  two  growths  show  that  a  number  of  disease-conditions  which 
are  commonly  considered  to  be  distinct  are  in  truth  closely  related, 
if,  indeed,  they  are  not  merely  variations  of  the  same  process.  The 
ulceration  must  be  classified  as  atheromatous,  and  the  sac  in  the 
fibrous  coat  as  an  aneurism,  for  the  intima  and  muscularis  were  broken 
through  and  the  vessel-wall  already  a  little  pouched  upon  its  outer  side. 
The  tendency  to  growth  like  a  toadstool  is  peculiar ;  the  same  dispo- 
sition to  proliferation  is  equally  plain  in  the  second  growth,  although 
it  was  less  extensive.  That  the  process  of  inflammation  was  an  im- 
portant factor  in  the  production  of  the  disease  is  certain,  for  nothing 
else  could  have  caused  the  ulceration  and  the  extensive  blood-clotting 
upon  the  cut  ends  of  the  muscular  coat.  An  interesting  feature  is 
that  the  connection  between  the  clot  and  portions  of  the  arterial  tissue 
is  so  intimate  that  it  is  impossible  to  say  where  the  one  ends  and  the 
other  begins.  The  fact  that  clots  within  vessels  are  not  mere  deposits 
upon  the  inner  surface  which  may  be  removed,  leaving  the  tube  in 
exactly  its  former  state,  is  well  known.  Threads  of  tissue  grow  out 
from  the  inner  wall  of  the  artery,  and  may  be  seen  running  through 
the  clot,  binding  it  firmly  in  the  situation  in  which  it  was  formed.*  It 
would  be  unreasonable  to  believe  that  a  vessel  suffers  no  injury  from 
the  formation  of  clots  within  it,  when  it  is  known  that  outgrowths  of 
tissue  from  the  intima  into  the  clot  are  a  common  accompaniment  of 
the  process.  It  is  my  belief  that  the  formation  of  clots  within  the 

*  Pathologische  Anatomic  von  E.  Ziegler,  Jena,  1892,  zweiter  Band,  Seite  59:  "die 
thrombotischen  Auflagerungen  bereits  von  der  darunterliegenden  Intima  mit  Bindegewebs- 
ziigen  durchwachsen  sind." 


58  THE   ORIGIN   OF   DISEASE. 

arterial  system  is  of  very  frequent  occurrence,  and  that  it  results 
from  a  great  many  of  the  diseases  and  even  disorders  to  which  men 
are  subject.  It  would  be  interesting  to  know  what  influence  clot- 
formation  may  have  in  the  production  of  the  thickenings  of  the  intima 
of  arteries,  especially  in  old  persons  and  those  past  middle  age.  In 
connection  with  the  growths  that  have  been  under  discussion  the  ap- 
pearances presented  by  Fig.  29  (see  description)  suggest  the  question, 
What  would  have  been  the  result  of  a  greater  duration  of  life  of  the 
patient  ?  The  minute  atheromatous  abscesses  and  areas  of  degenera- 
tion at  the  junction  of  the  intima  and  the  muscularis  could  not  have 
remained  as  they  were,  but  must  have  increased  in  size  until  they 
ruptured  and  the  cavities  discharged  their  contents  inwardly  into  the 
blood-stream  or  outwardly  through  the  fibrous  coat,  or  it  would  not 
seem  surprising  that  the  end  of  such  a  process  should  be  the  perfora- 
tion of  the  arterial  wall  and  the  discharge  of  blood  into  the  cranial 
cavity  to  produce  apoplexy. 

The  condition  which  has  been  described  as  tubercular  arteritis  is 
represented  by  Fig.  33.  The  vessel  looks  as  if  it  was  being  over- 
whelmed by  the  infiltration  of  cells  which  are  entering  from  its  out- 
side. There  is  nothing  that  suggests  the  existence  of  disease  of  truly 
vascular  origin,  but  the  appearance  is  that  the  vessel,  as  it  happened 
to  lie  in  a  tubercular  area,  was  involved  by  the  disease  in  the  course 
of  its  progress.  Tubercular  arteritis,  therefore,  has  no  real  existence, 
and  the  condition  is  nothing  but  the  involvement  of  the  vessels  by 
the  cellular  infiltration,  which  is  the  characteristic  of  the  tubercular 
process  everywhere. 

Veins. — Much  less  study  has  been  bestowed  upon  veins  than  upon 
arteries,  and  this  is  especially  the  case  in  regard  to  their  morbid  anat- 
omy. It  is  more  difficult,  therefore,  to  form  opinions  about  the  veins 
than  about  arteries,  for  there  is  in  comparison  so  little  pre-existing  in- 
formation to  serve  as  a  basis  upon  which  to  build.  The  literature  of 
disease  of  arteries,  both  that  found  in  text-books  and  that  found  in 
periodicals,  is  immense,  while  that  of  disease  of  veins  is  comparatively 
meagre.  Nevertheless,  certain  facts  about  the  veins  are  thoroughly 
well  established,  and  the  most  important  of  these  is  that  veins  are, 
from  their  very  nature,  less  subject  to  disease  than  are  arteries.  Of  the 
four  parts  of  the  circulatory  system,  the  heart,  the  arteries,  the  capil- 
laries, and  the  veins,  the  veins  alone  perform  a  passive  function.  Their 
sole  work  is  to  receive  the  blood  from  the  capillaries  and  return  it  to 
the  heart.  This  is  accomplished  by  forces  which  even  at  the  present 


FIG.  33. — TUBERCULAR  ARTERITIS.     (x  220.) 

From  a  man  forty-six  years  old  who  died  of  phthisis  :  a  minute  arteriole  lying  in  a 
tuberculous  area  of  the  lung.  There  is  some  clot  lying  in  the  lumen  of  the  vessel,  the 
walls  of  which  have  lost  all  differentiation  of  coats.  The  striking  feature  is  that  the  inner 
portion  of  the  vessel  is  that  which  is  most  nearly  natural,  while  from  the  outside  it  has 
been  invaded  by  the  infiltration  of  the  round  cells  which  constitute  the  greater  portion 
of  the  tuberculous  tissue.  The  whole  appearance  is  that  the  process  began  outside  and 
was  proceeding  thence  toward  the  inner  portion,  and  was  therefore  not  truly  vascular  in  its 
origin. 


.  33- 


THE  BLOOD-VESSELS.  59 

time  are  by  no  means  thoroughly  understood.  Further  than  this,  the 
fluid  they  carry  is  a  waste  product  which  they  receive  after  it  has  ac- 
complished its  function,  and  is  lifeless,  fit  only  to  be  returned  to  the 
great  mill  from  which  it  came,  to  be  worked  over  into  renewed  activity. 
There  is  no  more  common  disorder  as  life  advances  than  varicose 
veins  of  the  legs,  and  it  has  been  my  experience  to  find  that  in  cases 
where  the  arteries  are  greatly  diseased  the  veins  partake  in  the  process. 
It  seems  as  if  their  passive  nature  pursues  them  even  in  their  states  of 
disease,  and  that  they  become  diseased  most  often  when  some  other 
and  more  actively  disposed  part  of  the  organism  starts  the  train. 
When,  for  instance,  a  large  artery  like  the  femoral  becomes  thick  and 
rigid  from  the  deposit  of  calcareous  material,  its  accompanying  vein 
will  usually  be  found  to  be  similarly  diseased.  This  fact  I  discussed 
in  a  paper  published  some  years  ago,*  and  showed  that  atheroma  and 
calcareous  deposit  may  occur  in  a  vein  and  change  it  so  greatly  that 
it  cannot  be  distinguished  by  its  appearance  alone  from  an  artery. 
Figs.  34  and  35  are  reproduced  from  that  paper.  All  the  coats  are 
thickened,  the  intima  of  the  vein  being  thicker  than  that  of  the  artery 
(see  descriptions,  Figs.  34  and  35).  Fig.  36  represents  a  section  of 
the  vena  cava  of  a  man  fifty-seven  years  old  who  died  of  Bright's 
disease,  with  extensive  fibrosis  and  disease  of  the  arteries.  The 
vena  cava  is  seen  to  be  greatly  thickened,  degenerated,  and  of  a 
loose  texture,  and  some  of  its  vasa  vasorum  are  almost  closed  from 
endarterial  thickening  (see  description).  Figs.  37  and  38  show  a 
curious  and  interesting  instance  of  disease  of  a  vein.  The  first  rep- 
resents a  portion  of  a  vein  in  transverse  section,  and  was  published  in 
the  paper  just  mentioned.  Lying  opposite  each  other  in  the  wall  are 
two  growths.  One  of  these  is  represented  under  high  amplification 
by  Fig.  38.  There  are  irregularly  circular  nests  of  cells,  which  are  in 
many  respects  more  like  epithelium  than  like  connective  tissue.  The 
tendency  of  cells  to  arrange  themselves  in  this  manner  in  nests  in 
young  and  in  rapidly  growing  tissues  is  very  common,  and  is  fre- 
quently to  be  seen  in  skin  cancer,  in  the  healthy  skin  of  infants,  and 
in  embryological  tissues,  and  I  have  often  seen  such  nests  in  the 
walls  of  diseased  arteries  and  occasionally  in  diseased  heart-valves. 
The  resemblance  to  the  cell-nests  considered  so  characteristic  of  epi- 
thelioma  of  the  skin  is  very  close,  showing  that  great  care  must  be 

*  A  Study  of  the  Arteries  and  Veins  in  Bright's  Disease,  by  Arthur  V.  Meigs,  Trans- 
actions of  the  College  of  Physicians  of  Philadelphia,  June  6,  1888;  published  also  in 
The  Medical  Record,  New  York,  July  7,  1888. 


60  THE   ORIGIN   OF   DISEASE. 

exercised  in  pronouncing  an  opinion  from  microscopical  appearances 
alone  in  regard  to  the  malignancy  of  any  particular  growth.  The  dis- 
ease of  veins  offers  an  interesting  field  for  study,  especially  from  the 
side  of  pathology,  and  it  is  one  which  has  as  yet  been  very  imper- 
fectly investigated.  The  facts  that  have  been  adduced  tend  to  show 
that  the  veins  are  usually  involved  when  the  arteries  are  extensively 
diseased,  but  it  is  probable  also  that  it  will  be  found,  even  after  ex- 
haustive study,  that  disease  of  the  veins,  unless  more  extensive  than 
is  common,  plays  a  less  important  part  than  arterial  disease.  The 
passive  nature  of  the  function  of  the  veins,  and  the  fact  that  the  flow 
of  the  blood  is  from  a  great  number  of  small  tubes  into  a  constantly 
decreasing  number  of  greater  size,  make  the  friction  within  the  system 
an  always  decreasing  one,  and  render  them  less  liable  than  arteries  to 
disease. 

Capillaries. — The  normal  and  pathological  anatomy  of  capillaries 
will  be  discussed  in  connection  with  disease  of  the  heart  (page  63),  in 
which  organ  I  have  studied  them  with  more  profit  than  in  any  other 
part  of  the  body.  Of  the  three  kinds  of  vessels  of  which  the  vas- 
cular system  is  composed,  the  capillaries  are  the  most  difficult  to 
follow  and  understand.  This  difficulty  is  because  they  cannot  be 
examined  to  any  advantage  without  high  amplification,  and,  besides 
this,  the  material  of  which  they  are  composed  is  of  such  delicate 
structure  that  they  are  often  clouded  by  the  decomposition  of  the 
tissues  which  takes  place  before  or  after  death.  In  persons  dead  of 
typhoid  fever  and  other  diseases  which  cause  great  disorganization 
of  the  blood  and  general  softening  of  the  tissues,  microscopical  exam- 
ination often  yields  very  unsatisfactory  results  in  all  respects,  and 
delicate  parts  like  capillaries  cannot  even  be  seen. 

It  is  difficult  to  conceive  anything  that  could  be  more  important  to 
the  science  of  medicine  than  a  complete  comprehension  of  the  anatomy 
of  the  blood-vessels  and  an  understanding  of  their  diseases.  Such 
information  would  seem  to  promise  more  for  the  advancement  of  our 
knowledge  of  the  origin  of  disease,  and  especially  of  chronic  disease, 
than  anything  else.  Everything,  therefore,  that  adds  to  the  sum  of 
knowledge  of  this  subject  must  be  of  great  value.  The  illustrations 
and  description  of  the  anatomy  and  diseases  of  blood-vessels  which 
have  been  given  furnish  a  good  general  idea  of  the  forms  of  changes 
which  are  most  common  in  chronic  disease.  This  must  be  the  case 
because  they  are  representative  of  a  large  collection  of  sections 
gathered  in  the  course  of  many  years  in  hospitals  and  private  prac- 


FIG.  34. — VEIN  AND  ARTERY  SHOWING  THICKENING  OF  THE  INTIMA  AND  GENERAL 

ATHEROMA.     (X  6.) 

Femoral  artery  and  vein  from  an  elderly  man  who  died  of  Bright' s  disease.  Both 
vessels  were  converted  into  rigid  bony  tubes  by  calcareous  deposit,  and  had  to  be  treated 
with  acid  before  sections  could  be  cut.  The  artery  looks  broken,  the  intima  is  irregularly 
thickened,  and  there  are  spots  of  degeneration  of  the  muscular  coat.  The  intima  of  the 
vein  is  greatly  and  irregularly  thickened.  At  one  place  the  intima  and  muscularis  are 
broken  loose  from  the  fibrous  coat.  This  and  the  breaks  in  the  artery  either  resulted 
during  life  from  the  deposit  of  the  calcareous  material  or  occurred  after  death  in  removing 
the  vessels,  which  were  so  rigid  and  firmly  fixed  that  it  was  difficult  to  cut  them  loose. 
Fig.  35  shows  part  of  the  vein  more  highly  magnified. 

FIG.  35. — DISEASED  VEIN.     (X  22.) 

A  portion  of  the  vein  shown  in  Fig.  34,  more  highly  magnified.  ?',  intima ;  m,  mus- 
cularis, and  «,  adventitia.  Such  extensive  disease  with  great  thickening  of  the  intima  is 
probably  not  common  in  veins. 


FIG.  36. — THICKENED  AND  DEGENERATED  VENA  CAVA.     (X  44.) 

From  a  man  of  fifty-seven  years  who  died  of  Bright' s  disease,  e  is  a  section  of  the 
wall  of  the  vena  cava  magnified  about  four  diameters  ;  f  is  its  inner  and  g  its  outer  sur- 
face. At  g  the  outer  portion  of  the  adventitia  has  been  somewhat  separated  in  the 
process  of  preparation.  The  dotted  lines  indicate  the  portion  of  vena  cava  included  in 
the  larger  drawing  below  ( X  44)  ;  *  is  the  intima,  which  is  shredded  out  and  broken  as  the 
result  of  disease.  Below,  the  muscular  coat  is  very  loose-meshed,  and  at  n  is  replaced  by 
a  tissue  of  different  texture.  The  muscular  layer  is  much  thicker  than  natural.  The 
fibrous  coat  is  very  thick  and  loose-meshed,  and  there  are  vessels  in  it  (v).  The  two 
vessels  (v)  in  the  separated  portion  of  adventitia  are  so  greatly  thickened  inwardly  as  to 
be  almost  closed. 


FIG.  36. 


FIG.  37. — GROWTHS  IN  THE  WALL  OF  A  VEIN,     (x  50.) 

Part  of  a  vein  in  the  fat  layer  of  the  heart  of  a  man  of  fifty-four  years  who  died  of 
heart  disease.  The  vessel  was  somewhat  flattened  in  course  of  preparation,  and  therefore 
does  not  appear  as  circular.  There  are  two  growths,  one  upon  each  side  of  the  vein  ; 
one  of  these  (d]  consists  of  three  somewhat  circular  bodies,  and  it  is  represented  more 
highly  magnified  by  Fig.  38. 

FIG.  38. — GROWTHS  IN  THE  WALL  OF  A  VEIN,     (x  250.) 

Enlarged  view  of  the  growth  (d]  shown  in  Fig.  37.     There  are  three  circles  or  whorls,  and 
the  cells  are  very  like  epithelium. 


FIG.  37. 


I f"  >4V 

/'(./>' 


FIG.  38. 


THE   BLOOD-VESSELS.  61 

tice.  Clinical  observations  of  the  same  cases  were  made  concurrently, 
and  a  great  variety  of  diseases,  especially  of  chronic  diseases,  is  repre- 
sented. In  addition  to  the  graphic  demonstration  of  lesions  of  blood- 
vessels, which  includes  the  observation  that  the  intima  is  immeasura- 
bly more  often  the  seat  of  disease  than  are  the  two  other  coats,  several 
very  important  conclusions  are  reached. 

The  blood-vessels  always  undergo  changes  with  the  advance  of  life, 
and  these  changes  are  exactly  imitated  by  others  occurring  in  younger 
persons  as  a  result  of  disease ;  they  consist  principally  of  thickening 
of  the  coats  of  the  vessels,  especially  of  the  intima.  If  the  thickening 
be  extensive  it  always  reduces  the  size  of  the  calibre,  and  this  inevitably 
interferes  with  the  vessel's  function.  As  age  and  disease  produce 
identical  effects,  it  follows  as  a  corollary  that  it  is  frequently  difficult 
or  impossible  to  know,  from  the  appearances  alone,  whether  lesions 
are  those  which  belong  to  age  or  are  the  result  of  disease.  In  study- 
ing blood-vessels,  both  microscopically  and  with  the  unaided  eye,  the 
pathologist  always  has  to  contend  with  this  difficulty  of  deciding 
whether  departures  from  the  histological  standard  are  due  to  disease 
or  are  what  must  be  expected  to  be  present  in  consequence  of  the 
passage  of  time. 

Blood-vessels  are  especially  prone  to  disease,  owing  to  their  func- 
tion,— the  distribution  of  the  blood.  Besides  this,  they  are  present  in 
all  parts,  and  therefore  are  sure  to  come  within  the  range  of  every  dis- 
ease that  attacks  the  body,  no  matter  what  may  be  its  locality.  As 
blood-vessels  exist  everywhere,  they  are  likely,  owing  to  their  conti- 
nuity of  structure,  to  transport  disease  along  their  walls.  This  takes 
place  in  addition  to  the  carrying  of  disease  from  place  to  place  by  the 
blood  itself,  which  probably  is  effected  very  frequently. 

A  most  important  fact  is  that  there  are  no  peculiar  histological 
changes  of  blood-vessels  belonging  specifically  to  any  one  disease. 
Nothing  could  more  forcibly  illustrate  this  than  the  truth  which  is 
coming  to  be  pretty  well  known,  that  syphilitic  endarteritis  is  in 
every  respect  identical  with  endarteritis  arising  from  various  other 
causes.  The  endarteritis  deformans  which  is  so  common  in  old 
people,  and  which  is  often  found  in  various  parts  of  the  body  in 
Bright's  disease  and  in  chronic  heart  disease,  is  frequently  identical  in 
all  its  physical  characteristics  with  that  which  is  caused  by  syphilis. 
It  is  not  long  since  it  was  believed  that  certain  arrangements  of  the 
cells  and  certain  forms  of  thickening  of  the  walls  of  arterioles  could  be 
produced  only  by  syphilis,  and  that  it  was  not  difficult  for  any  one  who 


62  THE   ORIGIN   OF   DISEASE. 

had  attained  the  requisite  degree  of  skill  to  recognize  them  by  their 
peculiar  appearances  alone.  It  is  now,  however,  beyond  question  that 
there  are  no  specific  histological  lesions  which  belong  to  any  partic- 
ular disease.  Pathological  lesions,  both  gross  and  microscopical,  can 
help  to  a  conclusion  of  what  disease  is  being  dealt  with  only  if  they 
are  considered  in  a  general  way ;  the  state  of  the  blood-vessels  and 
changes  in  different  organs  must  be  judged  collectively  if  any  stable 
conclusion  is  to  be  reached. 

The  tendency  to  the  development  of  a  blood-supply  in  new  tissues 
is  well  known.  The  growth  of  such  blood-vessels  has  been  exten- 
sively studied,  and  their  peculiarities  of  origin,  even  in  clots,  thor- 
oughly elaborated.  The  formation  of  clots  and  their  organization  are 
probably  the  beginning  of  most  new  tissues  developed  as  a  result  of 
disease,  if  they  are  rapidly  produced.  When  new  tissue  is  developed 
slowly,  the  fibroid  cicatricial  tissue  of  which  it  is  composed  probably 
arises  without  any  clot-formation  as  the  first  step.  However  this  may 
be,  it  is  a  fact  that  even  in  adults  the  capacity  for  development  has  not 
been  extinguished,  and  under  the  stimulus  of  disease  is  often  set  in 
motion.  Of  this  no  more  striking  proof  could  be  adduced  than  is  fur- 
nished by  the  new  tissues  which  are  shown  by  the  illustrations.  The 
tissue  which  developed  between  the  two  layers  of  adherent  pericar- 
dium (Figs.  1 8,  19,  and  20)  and  in  the  lung-arteriole  (Figs.  23  to  27), 
thickening  it  inward,  and  the  vessels  developed  in  them  both,  show 
the  general  characteristics  of  the  process  in  a  most  satisfactory  man- 
ner. An  extraordinary  and,  at  present,  entirely  inexplicable  feature  of 
the  development  of  new  blood-vessels  is  the  occasional  formation  of 
solid  rods  (Figs.  15  and  20)  instead  of  tubes.  It  appears  as  if  the 
growth  that  is  started  by  disease  is  so  excessive  and  uncontrolled  that 
it  defeats  the  purpose  for  which  it  arose,  and  produces  a  useless  solid 
rod  where  a  tube  to  carry  liquid  is  needed.  This  strange  phenomenon 
is  worthy  of  careful  consideration,  although  as  yet  no  meaning  can  be 
attached  to  it.  The  striking  similarity  of  the  processes  of  develop- 
ment of  blood-vessels  in  new  tissues  under  the  stimulus  of  disease  and 
the  healthy  growth  of  blood-vessels  in  embryos  has  been  pointed  out 
(Figs.  23  to  27). 

The  fact  that  malignant  growths  may  be  closely  imitated  by  ar- 
rangements of  the  cells  occurring  in  disease  undoubtedly  non-malig- 
nant (Fig.  38)  has  an  important  practical  bearing.  It  shows  that  it 
may  be  difficult  to  conclude,  under  circumstances  which  not  infre- 
quently arise,  whether  in  a  given  case  disease  is  malignant  or  benign. 


CHAPTER    V. 

THE    HEART. 

IN  the  pursuit  of  pathological  studies  directed  especially  to  the 
investigation  of  Bright's  disease,  vascular  changes,  and  heart  disease, 
and  the  relations  of  these  morbid  processes  to  one  another,  I  have 
examined  a  great  many  hearts.  The  number  of  human  hearts  of 
which  sections  are  in  my  collection  is  eighty-nine,  and  in  most  in- 
stances these  are  accompanied  by  full  clinical  histories  of  the  patients. 
The  causes  of  death  include  violence  and  many  different  diseases,  and 
the  ages  ranged  from  an  early  embryological  period  to  three  weeks 
after  birth,  and  upward  to  old  age. 

Before  proceeding  to  discuss  disease  of  the  heart,  it  is  necessary  to 
describe  a  portion  of  its  anatomy.  The  blood-vessels  present  pecu- 
liarities which  make  the  cardiac  circulation  different  from  that  of  any 
of  the  other  organs.  Upon  this  subject  I  have  already  published  an 
essay  discussing  the  questions  involved.* 

Upon  the  surface  of  the  heart  there  are  numerous  arteries  and 
veins  of  ordinary  structure ;  they  have  three  coats,  and  the  muscularis 
has  circular  fibres.  Though  veins  with  three  coats  are  always  present 
on  the  surface,  they  are  rare  in  the  walls  of  the  heart,  where  three 
coats  are  found  only  in  veins  of  large  size,  the  smaller  ones  being 
composed  of  a  single  layer  of  endothelium,  which  is  in  appearance 
and  thickness  precisely  like  the  wall  of  the  smallest  capillary.  On 
the  other  hand,  the  arteries  have  three  coats,  the  circular  muscular 
fibres  being  easily  distinguishable,  until  the  size  of  the  vessel  is  little 
greater  than  that  of  the  capillaries  of  least  diameter.  The  process  of 
transition  from  arteriole  to  capillary  is  peculiar. 

The  transition  from  arteriole  to  afferent  capillary  is  in  strong  con- 
trast with  the  transition  from  capillary  to  efferent  vessel.  The  con- 
dition will  be  understood  by  examining  Fig.  39,  which  represents  the 
ordinary  appearance  of  a  return  vessel.  The  vessel  into  which  the 
smallest  capillaries  empty  is,  as  may  be  seen,  one  having  walls  no 

*  The  Microscopical  Anatomy  of  the  Human  Heart,  by  Arthur  V.  Meigs,  Transactions 
of  the  College  of  Physicians  of  Philadelphia,  April  I,  1891,  and  the  American  Journal  of 
the  Medical  Sciences,  June,  1891. 

63 


64  THE   ORIGIN   OF   DISEASE. 

thicker  than  the  smallest  capillaries,  and  is  in  structure  identical  with 
them.  The  small  capillaries,  too,  at  their  junctions  with  the  larger 
vessels  often  form  less  acute  angles  than  is  usual  at  points  where  ar- 
terioles  divide.  This  section  shows  two  places  where  efferent  capil- 
laries join  the  larger  vessels  at  right  angles,  thus  emptying  blood  into 
a  stream  flowing  at  a  right  angle.  Another  striking  point  is  that  effer- 
ent capillaries  seem  much  more  numerous  than  the  afferent,  great 
numbers  emptying  into  the  larger  vessels  within  small  areas,  while  at 
the  points  where  arterioles  break  up  the  number  of  capillaries  is  rela- 
tively much  less.  The  large  efferent  vessels  are  of  much  greater 
diameter  than  their  accompanying  arterioles,  but  whether  or  not  this 
was  the  case  during  life  is  impossible  to  decide,  for  it  may  be  that 
they  had  simply  remained  distended  with  blood  after  death. 

The  usual  condition  in  the  substance  of  the  heart  is  that,  of  parallel 
vessels,  the  one  a  carrier  of  venous  and  the  other  of  arterial  blood, 
the  arteriole  has  the  structure  commonly  described  as  proper  to  vessels 
of  that  nature,  while  the  venous  vessel  has  but  one  coat,  and  this  coat 
is  structurally  the  same  as  that  of  capillaries  of  the  smallest  size,  being 
formed  of  endothelium  alone. 

The  important  anatomical  point  is  that  in  the  walls  of  the  heart  the 
vence  comites  have  but  a  single  coat. 

The  distribution  of  the  capillaries  in  the  muscular  substance  of  the 
heart  is  well  known  up  to  a  certain  point :  histologists  thoroughly 
understand  that  the  arterioles  have  their  termination  in  capillaries 
which,  after  ramifying  among  the  muscular  fibres,  terminate  in  veins. 
To  say,  however,  that  the  whole  circuit  of  the  vessels  has  been  thor- 
oughly traced  out  as  has  that  of  the  capillaries  of  the  liver  and  kid- 
neys would  not  be  true,  for  in  the  works  upon  the  subject  the  ques- 
tion is  not  pursued  beyond  the  statement  that  the  muscular  fibres  are 
richly  supplied  with  capillaries.  The  capillaries  run,  of  course,  in  all 
directions  among  the  muscular  fibres,  parallel  with  and  between  them, 
at  acute  angles  across  them,  and  again  often  at  right  angles.  It 
becomes  necessary  now  to  approach  the  second  and  still  more  impor- 
tant part  of  the  subject, — the  appearance  and  structure  of  the  muscular 
fibres  themselves  in  their  more  intimate  relations  with  the  capillaries. 

Transverse  sections  of  muscle  show  the  position  and  number  of  the 
capillaries  and  their  relation  to  the  fibres  more  graphically  than  any 
others.  Under  these  circumstances  many  vessels  present  themselves 
in  the  form  of  circles,  or,  if  the  section  has  been  oblique,  as  elliptical. 
On  the  other  hand,  longitudinal  sections  may  present  an  almost  in- 


FIG.  39. — NORMAL  EFFERENT  CAPILLARIES  OF  THE  HEART.     (X  200.) 

From  a  negro  woman  of  forty  years  who  died  of  burns.     There  are  many  capillaries 

of  the  smallest  size  joining  to  form  a  large  efferent  vessel.     Some  of  the  junctions  form 

angles  which  are  not  acute,  and  there  are  even  right  angles  formed.     The  walls  of  the 

vessels,  from  the  smallest  to  the  largest  one  represented,  are  alike  in  structure  and  thick- 

•  ness.     The  dark  spots  are  endothelial  nuclei.     A  few  blood-corpuscles  are  seen. 

FIG.  40. — CAPILLARIES  WITHIN  THE  MUSCULAR  FIBRES  OF  THE  HEART.     (X  200.) 

From  the  same  tissue  as  Fig.  39  :  a  transverse  section  of  heart-muscle  fibres  and  of 
the  intervening  connective  tissue,  a  is  a  capillary  in  the  connective  tissue  ;  it  appears  as 
a  delicate  circle  of  endothelium.  b  is  also  a  capillary  in  the  connective  tissue,  but  it  is 
thickened  upon  one  side,  presenting  somewhat  the  appearance  of  a  seal-ring ;  this  is  be- 
cause a  flat  endothelial  nucleus  was  cut  across,  c  is  a  capillary  within  a  muscular  fibre,  d 
is  another  capillary  within  a  muscular  fibre  ;  it  is  distinctly  thickened  upon  one  side,  owing 
to  a  nucleus  in  its  wall.  The  muscular  fibres  are  not  circular,  but  present  very  irregular 
outlines. 


Fig.39 


THE   HEART.  65 

finite  variety  of  appearances.  It  would  be  impossible  to  give  an  ade- 
quate description  of  these  varying  appearances,  but  the  mere  mention 
of  their  existence  is  sufficient  to  remind  any  one  who  has  given  per- 
sonal attention  to  the  subject  of  the  truth  of  the  statement,  and  of  the 
further  truth  that  under  the  most  favorable  circumstances  longitudinal 
sections  of  vessels  are  less  satisfactory  to  study  than  are  cross-sections. 
Fig.  40  is  a  scale-drawing  of  a  single  field  under  the  microscope  of  a 
cross-section  of  heart-muscle.  It  shows  the  various  appearances,  but 
exaggerates  very  much  the  walls  of  the  capillaries  lying  within  the 
muscular  fibres ;  generally  they  are  invisible,  and  the  vessel  appears 
simply  as  a  hole  in  the  fibre.  It  is  easy  to  recognize  the  capillaries  in 
the  connective  tissue,  where  they  appear  as  minute  circles  with  walls 
of  exceeding  delicacy  and  of  equal  thickness  around  the  entire  circuit. 
In  a  few  of  them,  however,  the  walls  are  much  thicker  on  one  side 
than  on  the  other,  resembling  a  seal-ring  when  looked  at  from  the 
side.  These  thick  spots  are  caused  by  the  knife  having  cut  through  a 
nucleus  in  the  endothelium  of  which  the  wall  of  the  capillary  is  formed. 
A  closer  examination  of  the  drawing,  however,  brings  to  light  the  fact 
that  these  empty  circles  are  not  to  be  seen  in  the  connective  tissue 
alone,  for  they  exist  also  half  embedded  in  the  sides  of  the  muscular 
fibres,  and  even  entirely  within  them.  When  I  first  observed  these 
circles  lying  within  the  muscular  fibres,  and  at  their  edges  partially 
embedded  in  them,  I  did  not  know  what  explanation  to  offer  for  their 
appearance.  It  seemed  as  if  they  must  be  capillaries,  and  yet  the  fact 
that  they  were  closely  surrounded  by  the  muscular  tissue  made  it  dif- 
ficult to  determine  that  there  was  any  endothelial  wall  separating  the 
lumen  from  the  encircling  muscular  fibre.  Further  examination,  how- 
ever, brought  to  light  the  fact  that  in  places  endothelial  nuclei  could  be 
distinctly  seen  (Fig.  40),  and  study  of  a  great  number  of  sections  from 
different  hearts  showed  that  occasionally  the  endothelial  wall  could  be 
seen  in  capillaries  entirely  embedded  in  muscular  fibres,  thus  forcing 
me  to  the  belief  that  the  capillaries  not  only  enter  the  muscular  fibres, 
but  also  actually  penetrate  to  their  very  centres. 

In  order  to  prove  this  it  was  necessary  to  find  corresponding  ap- 
pearances in  longitudinal  sections.  As  has  been  stated,  longitudinal 
sections  do  not  yield  such  satisfactory  results  as  transverse  ones,  and 
the  appearances  are  much  more  difficult  to  interpret,  owing  to  the 
infinite  variety  of  forms  produced ;  but  the  examination  of  sections  in 
which  the  muscular  fibres  have  been  cut  longitudinally  shows  the  ex- 
istence of  the  cavities  as  definitely  as  the  cross-sections.  The  cavities 

5 


66  THE   ORIGIN   OF   DISEASE. 

are  generally  near  the  nuclei,  and  the  impression  is  given  that  capil- 
laries which  penetrate  muscular  fibres  pass  obliquely  through  them 
rather  than  for  any  great  distance  in  their  length. 

It  would  be  interesting  to  know  at  how  early  a  period  of  life 
capillaries  exist  within  the  muscular  fibres,  for  the  manner  in  which 
muscular  tissue  grows  from  cells  which  at  an  early  period  are  not 
to  be  distinguished  morphologically  from  the  cells  from  which  the 
other  tissues  arise  proves  that  capillaries  do  not  exist  within  the 
muscular  fibres  in  young  embryos.  The  presence  of  the  brown 
pigment  which  is  always  found  in  the  muscular  fibres  of  adult  hearts 
is  a  matter  requiring  investigation.  The  cavities  or  channels  which 
have  been  described  being  most  common  and  distinct  in  the  parts 
of  the  fibres  near  the  nuclei,  the  pigment  also  being  found  in  the 
same  position,  would  seem  to  indicate  that  this  pigment  is  in  intimate 
relation  with  or  derived  from  the  blood. 

The  fact  that  return  vessels  of  considerable  size,  whether  they  are 
called  veins  or  large  capillaries,  have  walls  of  the  same  thickness  and 
structure  as  the  smallest  capillaries,  is  evidence  of  the  thorough  pro- 
vision made  for  a  bountiful  supply  of  nutritive  material  to  the  heart. 
Vessels  of  this  character  must  have  a  double,  if  not  treble,  function : 
the  walls  are  so  thin  that  they  must  participate  directly  in  the  nourish- 
ment of  the  tissue ;  they  probably  act  as  reservoirs,  owing  to  their 
great  distensibility ;  and,  lastly,  they  certainly  are  carriers. 

A  brief  recapitulation  of  the  points  desirable  to  emphasize  may 
form  the  best  conclusion  to  the  consideration  of  this  anatomical  ques- 
tion,— a  question  which  viewed  by  itself  is  of  great  interest,  but  which 
when  considered  in  its  relation  to  pathology  seems  to  open  a  field  for 
labor  and  increased  knowledge  of  almost  boundless  extent.  They 
are  as  follows: 

1.  The  return  vessels  in  the  substance  of  the  heart,  except  a  few 
of  the  largest  size,  have  thin  walls  and  a  structure  identical  with 
that  of  the  most  minute  capillaries.     In  this  respect  they  present  a 
strong  contrast  with  the  arterioles,  as  the  latter,  even  when  of  very 
small  size,  are  similar  in  structure  to  large  arteries,  both  having  three 
coats. 

2.  At  points  where  return  vessels  are  formed  by  the  coming  together 
of  minute  capillaries,  the  number  going  to  form  the  return  vessel  is 
very  much  greater  than  at  corresponding  positions  where  arterioles 
break  up,  and  the  angles  formed  are  much  less  acute ;  even  right  angles 
occur  at  such  junctions  of  the  venous  vessels. 


3HT 

norjw 


FIG.  41. — DIAGRAM  SHOWING  DISEASE  OF  CAPILLARIES  OF  THE  HEART. 

a,  healthy  capillaries  which  appear  as  circles  with  walls  thicker  upon  one  side  ;  the 
thick  portion  occupying  about  one-third  of  the  circuit.  The  thicker  portion  represents  an 
endothelial  nucleus  cut  across,  the  rest  of  the  circle  is  delicate  endothelium.  In  general 
appearance  the  capillary  resembles  a  side  view  of  a  seal-ring.  £,  diseased  capillaries.  The 
nuclei  have  swollen  so  that  they  project  into  the  vessel,  reducing  the  calibre  in  size  and 
making  its  shape  irregular. 


Fu;.  41. 


C 


THE   HEART.  67 

3.  The  observation  of  the  presence  of  capillaries  in  the  fibres  of 
normal  human  heart-muscle  is  of  great  importance.  The  fact  that 
endothelial  nuclei  can  be  seen  in  them  in  almost  all  properly  prepared 
sections,  and  that  occasionally  even  the  whole  circle  of  the  endo- 
thelial wall  is  visible,  seems  to  be  sufficient  evidence  that  they  are 
capillaries. 

It  is  even  more  difficult  to  demonstrate  disease  of  the  capillaries  of 
the  heart  than  to  trace  out  their  distribution.  Fig.  41  is  a  diagram 
which  represents  in  contrast  the  natural  appearance  of  heart-capil- 
laries and  a  condition  of  them  which  is  sometimes  seen  when  the 
heart  is  diseased.  In  the  diseased  vessels  the  nuclei  are  swollen  and 
changed  in  shape ;  they  are  enlarged  and  rounded  so  that  they  project 
into  the  lumen  and  obstruct  it  (Fig.  41,  b).  This  condition  is  very 
common  in  Bright's  disease,  in  heart  disease,  and  in  other  forms  of 
chronic  disease.  Fig.  42  shows  two  capillaries  (b  and  c)  which  are 
narrowed.  The  effect  in  b  is  of  an  isolated  piece  of  capillary  drawn 
almost  to  a  point  at  both  ends,  while  c  is  a  narrow  neck  in  a  capillary 
through  which  no  natural-sized  red  blood-corpuscle  could  have  passed. 
At  the  point  of  narrowing  the  capillary  walls  are  slightly  thickened. 
There  are  blood-corpuscles  lying  in  this  vessel  close  to  the  neck,  which 
renders  it  easy  to  make  a  comparison  of  the  dimensions.  This  draw- 
ing is  a  faithful  representation  of  the  appearances  presented  by  the 
section  from  which  it  was  made.  It  may  be  said  that  this  narrow- 
ing of  the  capillaries  is  only  the  result  of  varying  directions  of  the 
plane  of  section,  but  such  does  not  seem  to  me  to  be  the  case.  I 
believe  it  to  be  an  actual  condition  of  disease.  None  of  the  muscular 
fibre  in  Fig.  42  is  healthy ;  most  of  it  is  granular  in  appearance  and 
the  cross-striae  are  indistinguishable,  but  here  and  there  are  scattered 
fibrils  in  which  the  striae  are  distinct.  A  curious  and  important  result 
of  disease  is  exemplified  by  the  two  bands  of  muscle  (x  and  j,  Fig. 
42)  which  run  at  right  angles  to  the  rest  of  the  muscular  tissue  in- 
cluded. A  somewhat  similar  condition  of  disease  is  represented  by 
Fig.  43,  in  which  the  muscular  fibres  are  generally  separated  from 
one  another  by  distinct  intervals  and  form  wavy  lines,  instead  of  being 
nearly  straight  and  disposed  in  close  bundles,  as  healthy  muscular 
fibres  of  the  heart  are.  The  connective  tissue  between  the  fibres  is 
evidently  greatly  increased,  for  in  healthy  heart-muscle  there  is  but 
little  connective  tissue.  The  condition  of  disease  is  one  of  fibrosis ; 
and  the  fibrous  tissue  has  forced  the  muscular  tissue  apart,  so  that 
individual  fibres  stand  by  themselves  and  have  been  dragged  about 


68  THE   ORIGIN   OF   DISEASE. 

and  distorted.  It  is  certain  that  muscle  so  distorted  must  have  been 
very  inefficient  in  its  action.  When  it  contracted  there  must  have 
been  great  waste  of  energy  in  pulling  the  curved  fibres,  and  great 
increase  of  friction  from  the  side  pressure  upon  the  fibrous  tissue. 
The  explanation  is  that  the  growth  of  fibrous  tissue  was  the  cause ; 
it  insinuated  itself  into  the  muscle,  pushing  the  fibres  apart  and  drag- 
ging them  out  of  line  until  they  became  isolated  and  wavy.  Portions 
of  muscular  fibre  so  distorted  as  the  two  right-angled  bands  repre- 
sented in  Fig.  42  must  have  been  useless,  and  the  wavy  fibres  in  Fig. 
43  very  inefficient. 

A  diseased  state  of  the  surface  layer  of  fat  of  the  heart  is  illustrated 
by  Figs.  44  and  45.*  The  two  pictures  were  drawn  with  the  same 
amplification  and  under  precisely  similar  conditions,  and  they  show 
two  different  stages  of  disease,  exhibiting  a  striking  contrast.  Con- 
densation and  fibrosis  of  the  fat  layer  of  the  heart  are  very  common  in 
persons  dead  of  various  chronic  diseases,  and  they  are  as  often  present 
in  cases  in  which  there  had  been  no  clinical  evidence  of  heart  disease 
during  life  as  in  those  in  whom  heart  lesions  had  been  recognized. 
The  changes  are  curious :  the  pericardium  is  thickened,  and  the  fat  so 
changed  that,  from  having  been  composed  of  a  collection  of  fine  circles 
looking  as  if  empty,  the  circles  become  more  coarse  and  lose  their 
discreteness,  until  finally  there  is  only  a  confusion  of  fibrous  threads, 
some  straight  and  some  curved,  intermingled  with  circles,  and  some- 
times there  is  even  new-formed  fibrous  tissue  rich  in  nuclei,  as  shown 
in  Fig.  45.  Fig.  44  illustrates  an  early  and  Fig.  45  a  more  advanced 
stage  of  fibroid  condensation  of  the  fat  layer  of  the  heart.  Through 
this  condensed  and  fibrous  fatty  tissue  run  the  blood-vessels,  and 
these  also  are  diseased  and  more  numerous  than  in  healthy  heart-fat. 
Whether  the  increase  in  numbers  is  due  to  the  condensation,  so  that 
more  vessels  appear  in  a  given  surface  in  the  section,  or  there  is  an 
actual  increase  of  them,  is  impossible  to  say,  but  the  evidence  is  in 
favor  of  an  actual  multiplication  of  vessels.  In  addition  to  their  in- 
crease in  number,  the  vessels  are  diseased ;  both  the  arterioles  and  the 
capillaries  are  thickened,  and  the  capillaries  in  places  (x,  Fig.  44)  are 
so  bound  up  with  the  fibrous  tissue  that  it  is  impossible  to  distinguish 
where  the  one  ends  and  the  other  begins.  The  effect  is  as  if  a  capil- 
lary ended  abruptly  in  a  mass  of  fibrous  tissue ;  and  it  is  not  necessary 
to  say  that  in  nature  no  blood-vessel  ever  has  an  ending,  but  always 
leads  on  into  another.  In  contrast  with  these  two  pictures  Fig.  I 

*  Figs.  45  and  43  are  from  the  same  heart. 


•utt 


SHT     'iO 


•\(h  &  tno 


iirfj    JA   J 


FIG.  42. — DISTORTION  AND  DISEASE  OF  THE  MUSCULAR  FIBRES  OF  THE  HEART  WITH 
NARROWING  OF  THE  CAPILLARIES,     (x  280.) 

From  a  man  of  fifty-four  years  who  died  of  organic  heart  disease.  The  drawing  is  of 
bands  of  muscular  fibres,  branching  and  ramifying  capillaries  of  various  sizes,  and  connective 
tissue,  m,  muscle,  the  greatest  portion  of  which  is  granular  in  appearance,  but  here  and 
there  are  fibrils  which  still  distinctly  show  cross-striae,  x  and  y,  muscular  bands  connect- 
ing at  right  angles  two  separated  portions  of  muscle.  Such  an  appearance  is  not  natural 
in  the  heart,  and  can  only  be  the  result  of  forcible  dragging  apart  of  the  fibres  by  the 
growth  of  fibrous  tissue,  a  is  a  normal  capillary  filled  with  blood-corpuscles,  b  is  a  por- 
tion of  a  capillary  which  is  too  narrow  to  have  performed  its  function,  for  its  diameter  is 
less  than  that  of  a  red  blood-corpuscle,  c  denotes  a  narrow  neck  in  a  capillary  through 
which  a  corpuscle  could  not  have  passed  ;  near  the  neck  and  lying  within  the  capillary 
are  blood-corpuscles.  It  may  be  thought  that  these  narrowings  were  the  result  of  the 
direction  of  section. 

FIG.  43. — FIBROID  HEART  WITH  DISTORTION  OF  THE  MUSCULAR  FIBRES,     (x  60.) 

From  a  man  of  forty-two  years  who  died  of  organic  disease  of  the  heart,  a,  new  and 
growing  fibrous  tissue  forcing  itself  between  the  muscular  fibres  (m).  The  fibrous  tissue  is 
rich  in  nuclei,  c,  a  capillary  running  at  right  angles  to  and  passing  sometimes  above,  and 
sometimes  below,  the  muscular  fibres.  The  muscular  fibre  is  pulled  open  and  distorted 
by  the  fibrous  tissue  to  such  a  degree  that  its  action  must  have  been  very  inefficient.  Fig. 
45  is  from  the  same  section. 

FIG.    44. — INFLAMMATION    CAUSING    CONDENSATION    OF   THE    FAT    LAYER    OF   THE 

HEART,     (x  60.) 

From  a  woman  of  forty  years  who  died  of  organic  disease  of  the  heart :  taken  from  a  dif- 
ferent portion  of  the  same  section  as  Fig.  I,  which  shows  normal  fat.  /,  thickened  peri- 
cardium ;  r,  a  capillary  forming  part  of  a  plexus  which  at  x,  adjacent  to  the  pericardium, 
is  diseased.  The  growth  of  fibrous  tissue  upon  the  under  side  of  the  pericardium  is 
continuous  with  the  capillaries,  so  that  it  is  impossible  to  say  at  what  precise  point  the  one 
ends  and  the  other  begins.  This  is  beyond  question  a  fibroid  change  involving  at  the 
same  time  the  pericardium  and  the  capillaries.  _/",  condensed  fat ;  the  rings  are  formed  by 
the  capsules  of  the  oil-cells,  which  are  less  discrete  and  not  so  nearly  circular  as  normal. 

FIG.    45. — INFLAMMATION    CAUSING    CONDENSATION    OF    THE    FAT    LAYER    OF    THE 

HEART,     (x  60.) 

From  the  same  section  as  Fig.  43.  /,  thickened  and  infiltrated  pericardium  ;  c,  a 
capillary,  and  v,  a  larger-sized  vessel  which  was  curved  so  that  it  has  been  cut  both 
longitudinally  and  across  its  calibre  ;  both  vessels  are  thickened,  f,  fat,  which  is  con- 
densed and  changed  by  inflammation  so  that  the  rings  are  all  small,  ill  defined,  and 
crowded  together,  presenting  a  marked  contrast  in  appearance  to  the  fat  in  Figs.  44  and  I. 
/,  an  area  of  round-cell  infiltration  beneath  the  pericardium, — one  stage  of  the  formation 
of  morbid  fibrous  tissue.  Figs.  I,  44,  45  present  three  different  conditions  of  heart- 
fat.  The  first  is  healthy,  the  second  diseased,  and  the  third  very  greatly  diseased. 


Fig.42 


THE   HEART.  69 

should  be  examined,  as  it  shows  healthy  heart-fat.  It  and  Fig.  44  are 
from  the  same  heart. 

Disease  of  the  fat  layer  of  the  heart  is  also  shown  by  Figs.  46  and 
47.  The  first  of  these  represents  a  section  through  the  entire  thick- 
ness of  the  ventricular  wall,  and  shows  how  the  natural  relative  pro- 
portion of  the  various  parts  is  changed.  Instead  of  the  fat  being  a 
thin  layer  upon  the  surface,  its  thickness  is  as  great  as  and  in  places 
even  greater  than  that  of  the  muscle.  Where  they  join,  fat  and 
muscle  are  much  commingled,  shreds  of  muscle  running  out  into  the 
fatty  substance.  Fig.  47,  which  is  an  enlarged  view  of  e,  Fig.  46, 
demonstrates  that  the  growth  of  the  fat  takes  place  at  the  expense  of 
the  muscle,  for  the  fat  can  be  seen  insinuating  itself  into  the  mus- 
cular tissue,  rending  the  fibres  and  fibrils  apart  and  destroying  them. 
The  appearances  presented  are  such  as  to  put  it  beyond  doubt  that 
the  process  of  fatty  infiltration  is  very  injurious  to  the  efficiency  of 
the  heart. 

In  the  description  of  the  changes  which  take  place  in  the  fat  layer 
of  the  heart,  it  has  been  pointed  out  that  the  fibrous  tissue  growth 
plays  an  important  part.  A  very  different  phase  of  cardiac  fibrosis 
is  shown  by  Fig.  52.  The  pericardium  is  greatly  thickened,  and  its 
tissue  contains  many  nuclei.  The  pericardial  sac  was  obliterated  by 
inflammatory  adhesion.  From  the  pericardium  bands  of  new  fibrous 
tissue  extend  into  the  substance  of  the  heart.  The  effect  produced 
is  like  that  of  water  flowing  in  a  stony  brook,  the  fibrous  bands 
being  the  water,  and  the  muscular  fibres  which  were  cut  across,  the 
stones.  When  water  flows  among  stones  it  finds  its  way  where  it  can, 
in  little  streamlets  resembling  the  bands  of  fibrous  tissue  extending 
inward  from  the  pericardium.  In  a  natural  condition  the  muscular 
fibres  of  which  the  heart  is  almost  entirely  composed  lie  adjacent  to 
one  another,  separated  only  by  a  very  small  amount  of  fibrous  tissue. 
The  condition  represented,  therefore,  is  very  morbid,  and  the  heart, 
although  it  was  of  about  twice  the  natural  size  and  had  during  life  a 
heaving  and  forcible  impulse,  must  have  been  a  very  inefficient  pump. 
The  question  of  the  true  meaning  of  enlargement  or,  as  it  is  named, 
hypertrophy  of  the  heart  is  most  important,  but  it  is  discussed  else- 
where (page  84).  In  Fig.  52  the  muscular  fibres  appear  to  be  com- 
pletely solid,  and  in  this  respect  they  are  in  strong  contrast  with  the 
disease  next  to  be  discussed. 

That  the  muscular  fibres  of  the  heart  are  sometimes  partially  hollow 
is  well  known,  and  the  disease  has  been  called  vacuolation.  Some 


70  THE   ORIGIN   OF   DISEASE. 

time  ago  I  published  an  essay  upon  the  subject,  in  which  it  was 
asserted  to  be  due  to  cystic  degeneration.* 

Figs.  48,  49,  50,  and  51  represent  variously  hollowed-out  muscular 
fibres.  It  has  already  been  shown  (page  65)  that  the  fibres  in  the 
healthy  human  heart  are  penetrated  by  capillaries,  and  are  not,  there- 
fore, as  is  commonly  supposed,  mere  solid  rods.  Fig.  48  is  a  drawing 
under  low  amplification  of  a  portion  of  a  papillary  muscle  of  the  left 
ventricle  from  the  heart  of  a  man  fifty-seven  years  old  who  died  of 
Bright's  disease.  It  is  seen  that  most  of  the  muscular  fibres  are  hol- 
lowed out  to  a  greater  or  less  degree,  and  there  is  some  increase  of 
the  intermuscular  fibrous  tissue.  The  contrast  of  these  hollow  fibres 
with  the  solid  ones  shown  in  Fig.  52  is  striking.  Fig.  49  represents  a 
few  of  the  fibres  included  in  Fig.  48,  more  highly  magnified  to  show 
the  details  of  their  structure.  The  destructive  process,  in  its  extreme 
development,  removes  the  whole  of  the  muscular  substance  from  the 
centre  of  the  fibre,  leaving  only  thin  outer  walls. 

A  curious  feature  is  that  the  nuclei  often  lie  loosely  in  the  cavities 
without  attachment  to  the  remaining  tissue, — a  condition  very  differ- 
ent from  natural.  The  disease  does  not  always  show  destruction  of 
the  entire  central  portion  of  the  fibres,  but  sometimes  eats  them  out 
irregularly,  producing  several  smaller  holes  in  different  parts  of  the 
fibres.  The  varieties  of  appearance  thus  produced  are  very  great,  and 
the  partitions  separating  the  cavities  are  sometimes  quite  thick,  and 
again  thin  and  almost  membranaceous.  They  may  be  incomplete, 
in  which  case  they  form  shelf-like  projections  partially  dividing  the 
cavities.  Fig.  50  is  a  longitudinal  view  of  a  fibre  from  the  same  heart 
as  Fig.  49,  and  shows  the  hollowing  of  the  central  portion  and  four 
nuclei  lying  loosely  in  this  cavity.  The  solid  walls  remaining  are  in 
places  so  far  degenerated  that  the  cross-striae  are  indistinguishable, 
but  in  others  they  are  distinct.  The  central  cavity  is  subdivided  by 
partitions  at  two  or  three  places,  and  it  contains  amorphous  material 
which  is  of  varying  degrees  of  density.  At  one  spot  the  partitions 
are  of  such  a  form  as  to  produce  the  effect  of  a  circular  opening, 
the  appearance  of  which  suggests  the  question  whether  it  is  a  dilated 
capillary  passing  into  or  through  the  fibre.  Fig.  5 1  represents  fibres 
in  transverse  section  from  the  heart  of  a  woman  forty  years  old  who 
died  of  organic  heart  disease.  The  appearance  is  somewhat  similar  to 

*  Cystic  Degeneration  of  the  Muscular  Fibres  of  the  Heart,  by  Arthur  V.  Meigs,  Trans- 
actions of  the  College  of  Physicians  of  Philadelphia,  1892,  and  The  American  Journal  of 
the  Medical  Sciences,  May,  1892. 


FIG.  46. — FATTY  INFILTRATION  OF  THE  HEART,     (x  3.) 

From  an  elderly  woman  who  died  of  dysentery  and  Bright's  disease.  The  section 
includes  the  entire  thickness  of  the  left  ventricle.  /  is  the  pericardium  and  g  the  endo- 
cardium ;  b  and  b  are  the  cut  edges.  It  is  striking  how  thick  the  fat  layer  is,  and,  on 
the  contrary,  how  thin  the  muscle,  which  has  diminished  owing  to  disease,  e  is  a  small 
vessel,  and  around  it  the  fat  has  infiltrated  the  muscle  so  that  it  is  shredded  out  and  torn, 
appearing  in  the  drawing  as  lines,  e  and  the  region  around  it  are  shown  more  highly 
magnified  in  Fig.  47. 

FIG.  47. — FATTY  INFILTRATION  OF  THE  HEART.     (X  50.) 

Enlarged  view  of  the  region  e  in  Fig.  46.  e  is  here  also  the  small  arteriole  ;  v,  a  vein 
filled  with  red  and  white  blood-corpuscles  ;  f  is  fat ;  h  is  muscular  fibre.  The  drawing 
shows  that  the  muscle  is  being  destroyed  by  the  growth  of  the  fat,  the  oil-globules  (circles 
as  seen  in  cross-section)  forcing  themselves  into  the  muscle  and  tearing  the  fibres  and 
fibrils  to  pieces. 


Fir..  46. 


I' K',.  47. 


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FIG.  48. — CYSTIC  DEGENERATION  OF  THE  MUSCULAR  FIBRES  OF  THE  HEART,     (x  60.) 

Section  of  a  papillary  muscle  of  the  left  ventricle,  including  a  portion  of  the  endocar- 
dium ;  from  a  man  sixty  years  of  age  who  died  of  gout  and  Bright' s  disease.  0,  £,  <:,  and 
d  are  cystic  fibres  correspondingly  lettered  in  Fig.  49.  The  drawing  shows  that  most  of 
the  fibres  are  hollowed  out,  some  more  and  some  less.  If  they  are  compared  with  those 
in  Fig.  52,  which  are  solid,  the  contrast  becomes  striking. 

FIG.  49. — CYSTIC  DEGENERATION  OF  THE  MUSCULAR  FIBRES  OF  THE  HEART. 

(X  340.) 

An  enlarged  view  of  muscular  fibres  from  the  same  section  as  Fig.  48.  a,  l>,  c,  and  d 
are  fibres  correspondingly  lettered  in  Fig.  48.  a  is  a  large  fibre  in  which  the  muscle  nu- 
cleus lies  free  in  a  cavity.  A  portion  of  this  fibre  is  divided  into  several  smaller  cavities 
which  contain  a  little  amorphous  debris,  b  denotes  two  closely  approximated  fibres,  or  a 
twin  fibre  ;  there  are  large  central  cavities  with  shadowy  threads  of  muscular  tissue,  which 
form  partitions  and  shelves  dividing  or  partly  dividing  the  spaces  into  several  cavities.  The 
external  rings  of  muscular  tissue  remaining  constitute  only  a  small  proportion  of  the  whole 
bulk  of  the  fibre.  At  the  point  of  junction  of  the  two  fibres  the  muscular  tissue  is  fused 
so  that  there  appears  to  be  only  a  single  wall,  c  has  a  large  cavity  eccentrically  placed, 
and  the  muscular  wall  is  still  quite  thick,  d  is  eaten  out  into  various  irregular  cavities  ; 
e  and /"are  fibres  still  solid  ;  they  show  that  the  muscular  substance  is  arranged  in  a  radiant 
striated  manner.  The  nucleus  of  e  is  of  very  irregular  shape. 

FIG.  50. — CYSTIC  DEGENERATION  OF  THE  MUSCULAR  FIBRES  OF  THE  HEART,     (x  340.) 

A  fibre  cut  longitudinally ;  from  the  same  tissue  as  Figs.  48  and  49.  Throughout  the 
whole  length  of  the  portion  included  in  the  drawing  the  fibre  is  hollowed  out  in  the  centre, 
so  that  it  forms  a  hollow  cylinder  whose  cavity  is  divided  by  partitions.  Within  the  cavity 
are  four  nuclei  lying  loosely  in  amorphous  material,  which  is  of  varying  density.  The 
muscular  tissue  still  left  and  forming  the  walls  of  the  cylinder  is  in  places  in  so  good  a 
state  of  preservation  that  the  cross-striae  are  distinct,  while  in  others  they  have  disappeared. 

FIG.  51. — CYSTIC  DEGENERATION  OF  THE  MUSCULAR  FIBRES  OF  THE  HEART,     (x  34°-) 

Transverse  sections  of  muscle  fibres  from  the  anterior  portion  of  the  heart,  near  the 
pericardial  covering ;  from  a  woman  forty  years  old  who  died  of  organic  disease  of  the 
heart.  The  process  is  seen  at  an  earlier  stage  than  in  the  preceding  figures.  There  are 
many  small  cavities,  and  fine  thread-like  divisions  between  some  of  them,  b  denotes  two 
fibres  or  a  twin  fibre,  and  in  the  portion  to  the  left  some  of  the  spaces  are  strikingly  like 
capillaries,  a  is  a  fibre  partly  solid  and  partly  eaten  away. 

FIG.  52. — FIBROID  HEART,     (x  60.) 

Section  of  the  anterior  portion  of  the  left  ventricle,  including  the  pericardium  ;  from  a 
man  sixty  years  old  who  died  of  gout  and  Bright' s  disease,  x  to  y  is  the  pericardium,  which 
is  enormously  thickened  and  consists  of  dense  fibrous  tissue  containing  many  nuclei.  From 
the  pericardium  and  continuous  with  it  are  bands  of  fibrous  tissue  (b]  which  pass  in  among 
the  muscular  fibres  (m)  :  the  appearance  is  like  that  of  water  flowing  among  stones  in  a 
brook.  The  muscular  fibres  (m)  which  have  been  cut  across  are  almost  all  separated  by 
an  interval  instead  of  touching  or  nearly  touching  one  another  as  is  natural,  and  the  space 
between  is  filled  by  fibrous  tissue  (/")  which  is  rich  in  nuclei.  The  muscular  fibres 
themselves  are  all  solid.  The  appearances  suggest  that  a  new  and  rapidly  growing  fibrous 
material  was  fast  extinguishing  the  muscular  tissue. 


Fig.49 


Fig.48 


b         d  c 


Fig.  50 


Fig.  5  2 


THE   HEART.  71 

that  of  Fig.  49,  but  the  disease  is  less  advanced.  There  are  numerous 
small  spaces,  but  there  is  still  a  good  deal  of  muscular  tissue  remain- 
ing. These  fibres  look  like  old  worm-eaten  wood.  The  material 
separating  some  of  the  cavities  (b)  is  a  thin  but  distinct  membrane, 
looking  exactly  like  the  endothelium  which  forms  the  walls  of  capil- 
laries. The  cavities  in  muscular  fibres  do  not  give  the  impression 
that  during  life  they  were  empty,  or  even  that  they  contained  only  a 
clear  liquid,  but  generally  there  is  within  them  more  or  less  material, 
without  distinguishable  structure,  which  is  represented  in  the  drawings 
by  dots.  Hollow  fibres  are  found  in  all  parts  of  the  heart,  but  they 
occur  more  frequently  near  the  serous  surfaces.  In  fibroid  hearts  they 
are  common,  but  generally  absent  from  the  most  fibroid  portions. 

It  is  not  possible  at  present  to  predict  from  any  clinical  manifesta- 
tions in  what  cases  hollowing  of  the  muscular  fibres  of  the  heart  will 
be  found.  The  examination  of  many  sections  has  demonstrated  the 
condition  to  be  absent  in  cases  clinically  recognized  as  brain  syphilis, 
sarcoma,  general  miliary  tuberculosis,  Bright's  disease,  pulmonary 
phthisis,  typhoid  fever,  pneumonia,  dysentery,  epithelioma  of  the 
bowel,  and  aneurism ;  and,  on  the  other  hand,  to  be  present  in  organic 
heart  disease,  Bright's  disease,  typhoid  fever,  ulcerative  endocarditis, 
and  in  young  infants  that  had  died  of  wasting.  Thus  it  is  seen  that  in 
cases  of  the  same  disease  it  is  sometimes  present  and  sometimes  absent. 
In  foundlings  dead  of  wasting  during  the  early  months  of  life,  the  mus- 
cular fibres  are  hollowed  in  some  instances  and  not  in  others.  In  a 
child  of  ten  who  died  of  amyloid  disease  of  the  heart,  lungs,  liver, 
spleen,  and  kidneys,  I  found  extreme  hollowing  of  the  muscular  fibres 
of  the  heart.  Some  of  the  fibres  in  this  case,  when  seen  in  longitu- 
dinal section,  presented  small,  bulbous-looking  swellings  at  points 
where  they  were  hollow,  making  it  appear  as  if  some  distending  pro- 
cess had  occurred  at  the  points  where  the  hollowing  existed. 

The  disease  has  been  called  vacuolation  and  hyaloid  degenera- 
tion, and  I  have  attributed  it  to  cystic  degeneration.  The  fact  that 
the  fibres  are  penetrated  by  capillaries  and  are  not  therefore  solid 
bodies,  together  with  the  appearance  of  the  cavities  and  the  nature 
of  their  contents  (see  page  75,  Fig.  58),  leads  inevitably  to  the  con- 
clusion that  the  capillaries  have  some  connection  with  the  production 
of  the  disease.  The  material  within  the  cavities  is  amorphous  or 
granular,  or  there  is  yellowish  pigment  in  irregularly  shaped  flakes, 
looking  as  if  suspended  in  a  liquid.  The  appearances  described  are 
those  of  partially  destroyed  blood,  and  if  the  contents  of  the  cavities 


72  THE   ORIGIN   OF   DISEASE. 

are  derived  from  the  blood  there  is  no  escape  from  the  conclusion  that 
they  are  of  the  nature  of  cysts.  In  Fig.  58  there  are  bodies  in  one 
of  the  hollow  fibres  which  look  like  partially  degenerated  blood-cor- 
puscles. If  the  cavities  contain  blood,  then  they  are  cysts  or  aneurisms 
according  as  they  had  still  a  connection  with  the  blood-stream  or 
were  cut  off  from  it.  The  appearance  of  the  cavities  indicates  that 
in  most  instances  they  were  closed  sacs  and  were  therefore  true 
retention  cysts,  although  in  such  a  cavity  as  one  of  those  in  Fig.  58 
there  may  have  been  still  an  opening  connecting  the  cavity  with 
the  blood-channels.  Figs.  53  to  58  exhibit  hollowing  of  the  mus- 
cular fibres,  attenuation  and  degeneration  of  them,  and  the  ramifica- 
tions of  the  capillaries  of  the  heart.  Fig.  53  shows  a  phase  of  hollow- 
ing of  the  fibres  of  which  I  have  not  seen  any  other  example.  The 
muscle  is  somewhat  granular,  but  a  few  of  the  cross-markings  can 
still  be  distinguished.  The  two  fibres  are  hollow,  and  this  is  very 
distinctly  to  be  seen,  as,  although  cut  longitudinally,  they  were  so  bent 
that  the  ends  were  cut  across.  These  cut  ends  appear  as  rings  of 
muscular  substance,  in  which  the  fibrillse  can  be  distinctly  seen  sur- 
rounding cavities.  In  the  section  from  which  the  drawing  was  made 
the  hollowing  has  proceeded  to  such  a  degree  that  it  is  in  some  in- 
stances impossible  to  decide  whether  a  given  hollow  cylinder  is  a 
blood-vessel  or  a  muscular  fibre.  There  can  be  no  doubt  that  those 
represented  in  the  drawing  are  hollow  muscular  fibres,  for  the  ring  of 
tissue  is  easily  recognized  as  muscular,  but  in  others  which  are  still 
more  degenerated  a  distinction  cannot  be  made.  Figs.  54,  55,  56,  and 
57  are  views  of  transverse  and  longitudinal  sections  of  fibres  from 
the  left  auricle  of  a  youth  of  seventeen  who  died  of  organic  heart 
disease.  There  was  complete  obliteration  of  the  pericardial  sac; 
the  heart  was  greatly  enlarged,  and  the  left  auricle  had  undergone 
fibroid  change  to  such  a  degree  that  it  was  difficult  with  the  naked 
eye  to  distinguish  any  muscular  tissue  in  it.  The  color  of  the 
auricle  was  a  light  grayish  brown,  instead  of  red.  The  fibres  are 
not  hollowed,  as  they  sometimes  are.  These  fibres  present  a  parallel 
in  miniature  to  what  occasionally  takes  place  in  the  heart  itself.  In 
a  natural  condition  the  muscular  fibres  of  the  heart  are  placed  close 
together,  generally  touching  one  another ;  disease  changes  this,  and 
by  the  growth  of  fibrous  tissue  or  by  other  cause  they  are  forced 
apart.  In  healthy  fibres  the  fibrillae  also  are  so  close  together  that 
there  are  no  intervals  between  them,  and  it  is  only  by  careful  study 
with  the  microscope  that  the  division  into  fibrillae  can  be  distinguished. 


FIG.  53. — HOLLOW  MUSCULAR  FIBRES  OF  THE  HEART.  (X  240.) 
From  a  woman  of  thirty  years  who  died  of  Bright' s  disease  :  there  was  cardiac  fibrosis, 
and  in  places  the  muscular  fibres  were  very  much  attenuated.  Three  fibres  are  included, 
cut  somewhat  in  their  length,  but  they  were  so  turned  that  their  ends,  two  of  which  are 
hollow,  are  seen  in  cross-section.  There  is  a  muscle  nucleus  in  the  upper  fibre.  The 
cross-markings  can  be  distinguished,  but  the  muscular  substance  is  somewhat  granular. 
Around  the  hollow  ends  the  subdivision  into  fibrillae  shows  very  distinctly. 

FIG.  54. — ATTENUATED  AND  DEGENERATED  MUSCULAR  FIBRES  OF  THE  HEART,  (x  240.) 

A  section  of  the  left  auricle  from  a  youth  seventeen  years  old  who  died  of  organic 
disease  of  the  heart :  the  fibres  are  cut  transversely.  Figs.  55,  56,  and  57  are  from  the 
same  section.  There  are  numerous  large  open  spaces  in  the  fibres,  and  the  fibrillae  appear 
as  dots  with  space  between.  The  small  delicate  rings  between  the  muscular  fibres  are 
capillaries,  a,  b,  and  c  are  the  fibres  represented  more  highly  magnified  in  Fig.  55. 

FIG.  55. — ATTENUATED  AND  DEGENERATED  MUSCULAR  FIBRES  OF  THE  HEART,  (x  400.) 

The  fibres  a,  b,  and  c  from  Fig.  54,  more  highly  magnified ;  correspondingly  lettered. 
The  large  space  in  b  is  sharply  outlined,  and  its  appearance  strongly  suggests  that  it  has  a 
wall  of  endothelium  ;  in  a  and  c  the  spaces  are  somewhat  irregular  in  shape.  The  appear- 
ance of  the  fibres  is  peculiar  ;  more  than  half  of  the  muscular  substance  has  disappeared, 
and  therefore  the  fibrillae  which  remain  appear  as  dots,  distinctly  separated  from  one  another. 
Between  the  dots,  however,  there  are  fine  threads,  so  that  the  appearance  is  like  that  of  an 
irregular  cobweb. 

FIG.  56. — ATTENUATED  AND  DEGENERATED  HEART  MUSCLE  WITH  CAPILLARIES 
WITHIN  THE  FIBRES.     (X  400.) 

From  the  same  section  as  Figs.  54,  55,  and  57  :  fibres  cut  longitudinally.  The  muscle 
looks  much  less  solid  than  usual,  and  the  fibrillae  are  separated  from  one  another.  The 
isolation  of  the  fibrillae  causes  the  cross-striae  to  be  unusually  distinct.  There  is  a  cavity 
at  either  end  of  the  nucleus  x,  and  the  nucleus  looks  as  if  it  had  been  indented  by  a 
capillary  tube  which  had  pressed  against  it  in  passing  obliquely  through  the  fibre,  y  is  a 
nucleus  which,  in  connection  with  the  opening  above  it,  looks  still  more  as  if  a  capillary 
had  passed  obliquely  through  the  fibre,  indenting  the  side  of  the  nucleus  in  its  course. 

FIG.  57. — CAPILLARIES  ENTERING  MUSCULAR  FIBRES  AND  RAMIFYING  AMONG  THEM. 

(X  240.) 

From  the  same  section  as  Figs.  54,  55,  and  56,  but  less  highly  magnified  than  the 
last,  showing  the  ramifications  of  the  capillaries  among  the  muscular  fibres  and  how  they 
appear  also  to  pass  into  them.  The  tenuity  of  the  fibres,  the  way  the  fibrillae  tend  to  stand 
apart,  and  the  great  distinctness  of  the  cross-markings  are  beautifully  shown. 

FIG.  58. — CYSTIC  DEGENERATION  OF  THE  MUSCULAR  FIBRES  OF  THE  HEART,    (x  240.) 

From  a  negro  man  of  thirty  years  who  died  of  organic  disease  of  the  heart,  m  de- 
notes portions  of  muscular  fibres  which  are  somewhat  granular  in  appearance  ;  other  fibres 
are  hollowed  out  and  changed  so  that  if  they  were  by  themselves  it  would  be  impossible  to 
recognize  them  as  muscle,  e  and  f  denote  hollow  fibres  whose  contents  appear  like  dis- 
integrated blood,  being  composed  of  granular  material  and  circular  or  partly  circular 
bodies  like  degenerated  red  blood-corpuscles,  c  is  a  fibre  with  thin  fibrous-looking  walls 
and  a  large  central  cavity  partly  filled  with  debris.  At  the  lower  end  of  c  the  semicircle 
formed  by  the  inturning  of  the  walls  appears  to  form  a  partition  in  the  cavity ;  above  is 
an  elliptical  opening  looking  like  a  capillary  cut  across.  The  conditions  suggest  a  minute 
aneurism,  the  blood  having  entered  by  the  elliptical  opening  and  torn  away  the  whole  of 
the  centre  of  the  fibre  to  form  a  cavity  for  itself. 


Fig.  53 


Fig.  56 


THE    HEART.  73 

In  the  drawings  the  fibrillae  are  seen  to  be  separated  from  one  another 
by  distinct  intervals  both  in  cross-section  and  in  longitudinal  section, 
and  thus  the  parallel  is  complete.  Fig.  54  represents  a  group  of 
muscular  fibres  in  cross-section  which  are  evidently  greatly  diseased. 
Their  average  size  is  much  less  than  natural,  and,  instead  of  being 
almost  solid,  they  are  of  open  structure,  the  fibrillae  being  separated 
from  one  another.  The  separation  of  the  fibrillae  varies  much  in  differ- 
ent fibres.  There  are  no  hollow  fibres  to  be  seen  like  those  in  Fig.  58. 
A  few  capillaries  are  visible  in  the  interspaces,  and  in  several  of  the 
fibres  are  circular  openings  which  probably  are  dilated  capillaries. 
Fig.  55  represents  three  fibres  included  in  Fig.  54,  more  highly  magni- 
fied to  show  details  of  the  structure.  These  are  the  capillaries  in  the 
fibres,  and  in  one  of  them  (£)  the  endothelial  wall  is  visible  in  the 
preparation,  but  this  feature  is  imperfectly  shown.  The  space  be- 
tween the  fibrillae  does  not  appear  to  be  empty,  but  contains  fine 
cobweb-like  threads  which  look  as  if  they  ran  from  one  fibrilla  to 
another.  This,  too,  the  drawing  fails  to  show  exactly  as  it  is  seen 
with  the  microscope.  Fig.  56  is  a  longitudinal  view  of  fibres  from 
the  same  section  as  Figs.  54  and  55.  It  shows  great  tenuity  of 
the  fibres,  which  are  of  less  than  average  width,  and  the  fibrillae  are 
separated  in  an  unnatural  way.  The  cross-striae  are  much  more  dis- 
tinctly seen  than  is  usual,  and  it  may  be  that  this  is  a  result  of  dis- 
ease, but  it  is  much  more  likely  that  it  is  due  to  the  free  passage  of 
light  through  the  spaces  between  the  fibrillae,  admitting  of  better 
illumination  than  can  be  had  in  healthy  muscle,  in  which  the  fibrillae 
are  in  contact.  The  spaces  between  the  fibres  are  filled  with  fine 
fibrous  tissue.  The  muscle-nuclei  have  spaces  at  both  their  ends,  as 
is  usual  in  all  heart-muscle  except  that  of  very  young  infants,  but  in 
two  of  those  here  depicted  (x  and  y]  the  shape  of  the  nuclei  and  of 
the  spaces  in  which  they  lie  is  such  as  to  suggest  that  capillaries 
passed  through  the  fibres,  indenting  the  nuclei  upon  the  side.  In  one 
of  the  fibres  (y)  this  appearance  is  very  distinct,  but  it  is  only  moder- 
ately well  shown  by  the  drawing.  These  spaces  at  the  poles  of  the 
nuclei,  which  are  present  in  some  degree  in  almost  all  pathological 
hearts,  are  commonly  attributed  to  what  has  been  named  brown 
atrophy.  The  nature  of  the  amorphous  and  pigmented  material  and 
the  fact  that  the  fibres  are  penetrated  by  capillaries  make  it  probable 
that  the  material  is  derived  from  the  blood,  and  that  the  spaces  have 
some  connection  with  the  circulation.  Fig.  57  is  a  group  of  fibres 
from  the  same  section  as  Fig.  56,  less  highly  magnified,  and  it  shows 


74  THE   ORIGIN   OF   DISEASE. 

the  separation  of  the  fibrillae,  which  are  woven  in  and  out  in  the  fibres 
like  the  strands  of  a  plaited  rope.  The  cross-striae  are  very  distinct, 
and  the  spaces  between  the  fibres  are  filled  with  fibrous  tissue,  which 
is  present  in  unnaturally  great  amount.  The  special  feature,  however, 
of  this  illustration  is  the  exhibition  it  makes  of  the  ramifications  of 
the  capillaries.  Owing  to  the  tenuity  of  the  muscle  and  the  separa- 
tion of  the  fibrillae  permitting  of  the  passage  of  light  with  unusual 
freedom,  these  can  be  seen  with  a  distinctness  that  I  have  not  noticed 
in  any  other  tissue.  The  capillaries  as  seen  with  the  microscope 
appear  to  pass  directly  into  the  fibres,  and  this  effect  is  well  repro- 
duced by  the  drawing.  The  four  sections  last  described  illustrate  a 
very  curious  form  of  fibroid  disease  of  the  heart.  The  heart  from 
which  the  sections  were  taken  was  inflamed,  for  there  was  great  in- 
crease of  the  intermuscular  nuclei ;  it  was  generally  fibroid  and  greatly 
hypertrophied,  and  the  pericardium  was  adherent.  In  addition  to  all 
this  there  was  such  extensive  fibrosis  of  the  auricles  that  they  looked 
more  like  connective  tissue  than  like  muscle,  for  the  tissue  was  grayish- 
white  instead  of  red  like  healthy  muscle.  Microscopical  examination 
demonstrated  extensive  disease  of  the  endocardium  and  of  the  peri- 
cardium, and  the  auricular  walls  were  composed  of  thickened  endo- 
cardium and  pericardium  with  only  a  thin  stratum  of  muscle  between. 
It  seems  impossible  that  the  auricles  could  have  had  any  contractile 
power  left.  The  marked  peculiarity  of  the  fibroid  disease  in  the  case 
lies  in  the  condition  of  this  thin  remnant  of  the  auricular  muscular 
tissue. 

In  Figs.  54,  55,  56,  and  57  there  is  no  hollowing  out  of  the  mus- 
cular fibres,  nor  are  they  granular  or  fatty.  The  peculiarity  consists  in 
their  attenuation  and  in  the  separation  both  of  them  and  of  the  fibrillae 
from  one  another.  The  substance  that  filled  the  spaces  between  the 
fibres  and  between  the  fibrillae  must  have  been  something  of  the  nature 
of  fibrous  tissue.  The  condition  is  one  I  have  never  seen  developed 
to  an  equal  extent  in  any  other  case.  Fig.  58  is  heart-muscle  from  a 
man  thirty  years  old  who  died  of  organic  heart  disease.  There  are 
parts  of  fibres  included  which  can  still  be  recognized  as  muscular 
tissue,  although  the  cross-striae  do  not  show  very  well  and  it  is  some- 
what granular.  Most  of  the  fibres,  however,  are  so  diseased  as  to  be 
past  recognition,  being  composed  of  large  central  cavities  with  thin 
fibrous  walls.  These  walls,  unlike  those  of  the  fibre  shown  by  Fig.  50, 
do  not  look  in  the  least  like  muscular  tissue,  but  are  purely  fibrous 
in  their  composition.  The  effect  is  as  if  the  whole  of  the  muscular 


THE   HEART.  75 

substance  had  been  removed,  leaving  behind  it  an  empty  shell.  Some 
of  the  fibres  contain  within  their  cavities  circular  bodies  resembling 
partially  disintegrated  blood-corpuscles.  In  the  drawing  this  pecu- 
liarity is  somewhat  exaggerated,  for  the  circular  bodies  can  be  seen 
with  the  microscope  only  after  careful  study.  At  positions  where  the 
fibres  are  most  hollow  they  are  swollen,  producing  bulbous  enlarge- 
ments ;  this  is  seen  in  several  of  the  fibres.  Such  swelling  could 
result  only  from  distention  of  the  shell  of  the  fibre  by  the  accumu- 
lation of  some  material  within  the  cavity.  At  the  upper  end  of  one 
fibre  (c)  which  is  completely  hollowed  and  presents  a  distended  appear- 
ance, there  is  an  elliptical  opening  which  looks  as  if  a  capillary,  cut 
obliquely,  had  entered  the  cavity.  Taken  together,  the  appearances 
of  these  fibres  lend  strong  support  to  the  view  that  the  hollowing  of 
the  muscular  fibres  is  a  true  cystic  degeneration  and  that  the  cysts 
originate  from  the  capillaries  within  the  fibres.  Figs.  53  to  58,  all 
included  upon  the  same  plate,  make  a  good  demonstration  of  the 
extreme  variability  in  size  of  the  muscular  fibres  of  the  heart.  One 
of  the  fibres  in  Fig.  53  is  the  largest  of  any  shown.  In  comparing 
them  it  must  be  kept  in  mind  that  Figs.  55  and  56  are  almost  twice 
as  much  magnified  as  the  other  four.  Extreme  tenuity  of  the  fibres 
and  reduction  in  their  size  are  among  the  most  common  and  striking 
peculiarities  of  long-standing  disease  of  the  heart.  These  changes 
seem  to  belong  especially  to  those  cases  in  which  there  was  inflam- 
matory disease  for  a  long  time  before  death.  Another  strange  and 
at  present  inexplicable  feature  is  that  in  cases  of  fibrosis  the  fibres  are 
sometimes  hollow,  and  again  they  are  more  solid  in  appearance  than 
in  histological  tissue. 

Figs.  59  to  62  illustrate  cystic  disease  of  the  heart.  A  full  account 
of  the  case,  which  was  one  of  cystic  disease  of  the  heart,  liver,  spleen, 
and  kidneys,  has  already  been  published,*  but  with  very  inadequate 
illustrations.  Fig.  59  shows  many  cavities.  These  are  of  different 
sizes  and  are  variously  placed,  sometimes  singly,  at  other  times  close 
together.  In  some  places  only  thin  membranous  walls  separate  one 
cavity  from  another,  and  in  others  two  or  more  cavities  are  joined, 
being  only  partially  separated  by  broken  or  incomplete  partitions. 
Examination  of  the  section  with  greater  amplification  shows  that  the 
heart  is  fibroid,  the  fibrous  increase  being  greatest  near  the  endo- 


*  Cystic  Degeneration  of  the  Heart,  Spleen,  Liver,  and  Kidneys,  by  Arthur  V.  Meigs, 
Journal  of  Anatomy  and  Physiology,  vol.  xxvii. 


76  THE   ORIGIN   OF   DISEASE. 

cardium  and  around  the  papillary  muscles.  The  fibres  are  pushed 
apart,  and  there  is  increase  of  the  intermuscular  nuclei,  showing  that 
there  had  been  inflammation.  The  cysts  are  usually  surrounded  by 
muscular  tissue,  there  being  no  differentiated  cyst-wall.  In  places, 
however,  there  is  a  very  distinct  cyst-wall  quite  different  in  its  consti- 
tution from  the  muscular  tissue.  This  consists  of  a  fine  structureless 
or  fibrous  membrane,  the  so-called  basement  membrane,  and  in  it 
are  flattened  nuclei,  like  the  common  endothelial  nuclei  of  capillaries 
and  of  the  intima  of  arteries.  A  differentiated  cyst-wall  is  more  often 
found  in  small  cysts  than  in  the  larger  ones ;  and  if  there  is  any  cyst- 
wall  in  those  of  large  size  it  has  generally  been  broken,  thus  giving 
the  impression  that  the  membranous  walls  had  been  torn  through 
and  destroyed  as  the  cavities  grew  larger  from  the  increase  of  the 
quantity  of  liquid  contents.  In  places  there  is  marked  condensation 
of  the  muscular  tissue  around  the  cysts,  and  here  and  there  portions 
of  cyst-contents,  consisting  of  structureless  material,  have  been  in- 
cluded. The  amount  of  solid  material  within  the  cysts  must  have 
been  very  small, — a  few  flocculi  in  the  liquid.  It  is  remarkable  that 
there  should  have  been  in  the  same  case  cystic  degeneration  of  four 
of  the  most  important  organs  of  the  body,  and  it  is  improbable  that 
the  cysts  had  different  modes  of  origin.  The  cause  that  produced 
them  in  one  organ  produced  them  in  all.  Cysts  are  classified  in  two 
great  divisions, — true  cysts  and  pseudo-cysts,  or  spurious  cysts.  The 
latter  are  those  which  arise  in  the  substance  of  the  organs  or  tissues 
owing  to  hemorrhage  or  disintegration  or  other  pathological  process, 
while  true  cysts  have  their  origin  in  the  abnormal  dilatation  of  a  pre- 
existing tubule  or  cavity.  It  does  not  seem  likely  that  the  cavities 
shown  in  the  illustrations  are  spurious  cysts,  for  such  an  assumption 
is  negatived  both  by  their  appearance  and  by  the  fact  that  true  cysts 
having  precisely  the  appearances  of  these  are  well  known  to  occur  in 
the  kidneys  and  in  the  liver.  It  is  probable  that  the  cavities  in  the 
four  organs  had  a  common  mode  of  origin ;  but,  so  far  as  the  spleen 
and  the  heart  are  concerned,  except  the  blood-vessels  and  the  lym- 
phatics there  are  neither  pre-existing  tubules  nor  cavities  which  could 
undergo  abnormal  dilatation.  The  cavities  are  not  pseudo-cysts,  and, 
this  being  the  case,  they  must  be  true  cysts,  originating  in  blood- 
vessels or  lymphatics.  Of  diseases  of  lymphatics  there  is  as  yet  very 
little  known,  but  cystic  dilatations  of  blood-vessels  resulting  in  the 
production  of  aneurism,  varix,  and  capillary  aneurism  are  among  the 
most  common  of  pathological  processes. 


FIG.  59. — CYSTIC  DEGENERATION  OF  THE  HEART.     (X  7-) 

From  a  man  of  seventy-seven  years  who  died  of  cystic  disease  of  the  heart,  liver,  spleen, 
and  kidneys.  The  cysts  vary  in  size  and  are  irregular  in  shape  ;  some  of  them  are  sepa- 
rated only  by  thin  membranous-looking  partitions.  The  walls  of  some  are  in  parts  con- 
densed and  thicker  than  the  tissue  elsewhere,  c  is  a  cyst  which  with  the  surrounding 
tissue  is  represented  more  highly  magnified  in  Fig.  60.  Figs.  60  and  6 1  are  from  the 
same  section,  and  Fig.  62  is  from  another  section  of  the  same  tissue. 

FIG.  60. — CYSTIC  DEGENERATION  OF  THE  HEART,     (x  50.) 

An  enlarged  view  of  the  region  c  in  Fig.  59.  The  cyst  is  a  large  opening  which  to  the 
left  has  no  apparent  outlet,  while  to  the  right  it  is  continued  into  a  long  narrow  channel. 
e  is  a  delicate  membrane-like  endothelium,  which  is  to  be  seen  upon  both  sides  of  the 
narrow  channel  and  to  some  extent  in  the  larger  portion  of  the  cyst.  In  this  membrane 
are  a  number  of  bead-like  cells  which  resemble  endothelium.  x  is  the  centre  of  the  region 
represented  more  highly  magnified  by  Fig.  6l. 

FIG.  61. — CYSTIC  DEGENERATION  OF  THE  HEART,     (x  250.) 

The  region  x  in  Fig.  60,  more  highly  magnified,  y  corresponds  in  position  with  the 
end  of  the  leader  x  in  Fig.  60.  in,  muscular  tissue,  some  upon  both  sides  of  the  chan- 
nel being  included.  It  is  degenerated,  in  places  the  cross-markings  being  visible  and 
again  having  disappeared,  e  is  the  endothelium,  and  it  is  well  defined  upon  both  sides  of 
the  channel  and  contains  a  number  of  nuclei.  At  a  is  a  nucleus  which  is  histologically 
typical  ;  it  is  enclosed  by  the  endothelial  plate,  which  has  split  into  two  layers  to  surround 
it  like  a  frame. 

FIG.  62. — CYSTIC  DEGENERATION  OF  THE  HEART,     (x  50.) 

From  another  section  of  the  same  tissue  as  the  preceding,  showing  the  breaking  down 
of  the  substance  of  the  heart.  Above  is  a  cyst  which  is  nearly  circular  and  does  not  seem 
to  be  connected  with  any  other.  Below  is  an  irregularly  shaped  and  imperfectly  divided 
collection  of  cysts  with  shreds  and  fibres  of  degenerated  muscular  tissue  to  form  such 
walls  as  exist  to  separate  one  cavity  from  another. 


Fi.   53. 


Fig.  60 


Fig.  62    £ 


THE   HEART.  77 

Figs.  60  and  61  represent,  more  highly  magnified,  one  of  the  cysts 
in  Fig.  59.  The  larger  cavity  in  Fig.  60  is  prolonged  into  a  narrow 
channel,  and  both  the  cavity  and  the  channel  are  partly  lined  with  a 
membrane  which  is  in  every  respect  identical  with  the  endothelium 
which  forms  the  walls  of  capillaries.  Fig.  6 1  is  a  portion  of  the 
channel  still  more  magnified,  and  it  shows  the  membranous  endothelial 
lining  and  the  flattened  nuclei  peculiar  to  that  sort  of  tissue  (see 
description  of  plate).  Fig.  62  is  from  another  section  of  the  same 
tissue,  and  it  shows  cavities  with  shreds  of  tissue  irregularly  sepa- 
rating them, — an  early  stage  of  the  cyst-formation.  These  partitions, 
when  examined  with  greater  amplification,  will  be  seen  to  be  formed 
of  muscular  tissue  and  portions  of  fibrous  material.  The  effect  is  as 
if  a  liquid  had  accumulated  and  had  increased  in  quantity,  separating 
and  tearing  the  muscular  fibres  apart  and  destroying  them.  The 
parallel  with  what  takes  place  upon  a  large  scale  in  arterial  aneu- 
rism is  very  close.  In  aneurism  the  distending  force  is  so  great  that 
even  so  rigid  a  barrier  as  the  bony  spinal  column  must  yield  if  it  hap- 
pens to  be  in  the  way.  It  seems  as  if  there  must  be  some  connection 
between  the  hollowing  of  the  muscular  fibres  which  has  been  described 
and  cystic  disease. 

Study  of  the  gross  post-mortem  appearances  with  the  clinical  his- 
tories of  eighty-nine  cases  and  microscopical  examination  of  the  hearts 
lead  to  a  number  of  interesting  observations.  The  heart  in  the 
earlier  periods  of  life  differs  from  the  heart  in  old  age;  it  changes 
gradually,  but  disease  sometimes  makes  the  young  heart  very  like  that 
of  more  advanced  life.  At  an  early  embryological  period  no  cross- 
striae  can  be  seen  in  the  muscle  cells,  and  even  in  young  infants  the 
striae  are  not  easy  to  distinguish  and  have  not  the  appearance  that 
they  acquire  during  adult  life.  In  youth  the  heart  is  of  a  closely  knit 
texture,  the  muscular  fibres  being  placed  so  close  together  that  it  is 
difficult  to  distinguish  an  interval  between  them,  and  there  is  scarcely 
any  fibrous  tissue  to  be  seen  except  in  the  spaces  where  the  blood- 
vessels lie.  As  life  advances,  fibrous  tissue  accumulates  and  the  fibres 
become  separated.  To  a  certain  extent  this  change  must  be  con- 
sidered as  histological  and  natural  to  the  advance  of  life,  but,  as  has 
been  shown  in  the  preceding  pages,  it  is  often  the  result  of  disease. 
It  has  been  said  that  that  curious  form  of  degeneration,  hollowing  of 
the  muscular  fibres,  may  occur  in  very  early  life.  It  has  been  found 
in  infants  a  few  months  old,  and  in  children  of  from  nine  to  twelve 
years,  and  sometimes  the  fibres  are  swollen  and  bulge  at  the  points  of 


78  THE   ORIGIN   OF   DISEASE. 

greatest  hollowing,  just  as  they  have  been  shown  to  do  in  older  per- 
sons. It  has  already  been  stated  that  hollowing  of  the  muscular  fibres 
sometimes  occurs  to  such  a  degree  and  in  such  form  that  it  may  be 
impossible  with  certainty  to  distinguish  whether  a  given  hollow  cylin- 
der in  a  section  of  the  heart  is  a  muscular  fibre  or  a  blood-vessel.  The 
hollowing  of  the  muscular  fibres  might  be  thought  to  be  a  result  of 
fatty  degeneration,  but  testing  with  osmic  acid  shows  that  such  is 
not  the  case;  besides  which,  the  hollowed  fibres  do  not  look  like 
fatty  degeneration.  Hollowing  of  the  fibres,  fibrosis,  and  increase  of 
the  intermuscular  nuclei  often  exist  together  in  the  same  case.  An 
important  observation  is  that  which  was  made  in  connection  with  the 
capillary  nuclei,  which  appear  to  enlarge  so  as  to  obstruct  if  not  shut 
off  the  capillaries.  In  sharp  contrast  with  the  hollowing  of  muscular 
fibres  is  the  unusually  solid  appearance  they  sometimes  present,  even 
in  hearts  that  are  very  fibroid  and  diseased.  (Fig.  52.)  Condensation 
of  the  fat  until  hardly  any  fat  cells  are  left  and  it  becomes  a  fibrous 
tissue  containing  a  greatly  increased  number  of  capillaries  is  one  of 
the  commonest  changes  in  hearts  that  have  been  long  subjected  to 
chronic  inflammation. 

The  shredding  apart  of  the  muscular  fibres  and  the  fact  that  they 
become  so  distorted  as  to  run  at  right  angles  to  one  another,  and  at- 
tenuated and  narrow  (Figs.  42  and  56),  have  already  been  mentioned. 
These  conditions  are  very  common  in  fibroid  hearts  and  in  those  that 
have  been  subjected  to  long-standing  inflammation  :  such  organs  must 
be  very  ineffective  pumps.  When  a  heart  has  been  in  a  condition  of 
chronic  inflammation,  one  of  the  most  striking  changes  that  take 
place  is  the  great  increase  of  the  number  of  intermuscular  nuclei. 
This  is  one  of  the  commonest  appearances  discovered  in  the  hearts 
of  those  dead  of  chronic  disease.  Granular  degeneration  of  muscular 
fibres  is  spoken  of  in  pathological  works  as  though  it  were  one  of  the 
commonest  and  best  known  of  diseases.  In  truth,  however,  it  is 
generally  very  difficult  to  decide  in  a  given  section  whether  a  certain 
indistinctness  of  the  cross-striae  and  a  slight  granular  or  powdery 
look  of  the  fibres  are  really  due  to  granular  degeneration  or  only  to 
faulty  preparation  of  the  section.  Among  the  eighty-nine  hearts  of 
which  I  have  sections,  there  is  one  in  which  granular  degeneration  has 
proceeded  so  far  that  the  individual  granules  can  be  seen  as  blackish 
dots.  Such  an  appearance  is  certainly  pathological,  and  muscular 
fibre  so  affected  must  be  inefficient  in  function.  In  the  case  of  a  child 
of  twelve  who  died  having  amyloid  degeneration  of  the  liver  and 


THE   HEART.  79 

kidneys,  and  in  whom  there  had  been  long-standing  organic  disease 
of  the  heart,  the  pericardium  was  found  adherent  to  such  a  degree  as 
to  have  obliterated  the  pericardial  sac.  In  the  fibrous  tissue  over  the 
heart,  which  was  composed  of  the  thickened  pericardium  and  new 
growth  which  bound  the  two  layers  of  the  pericardium  together,  was 
material  which  resembled  amyloid  deposit.  Amyloid  disease  of  the 
heart  is  not  described  as  being  of  frequent  occurrence,  but  it  is  highly 
probable  that  if  sought  for  it  would  be  found  to  be  much  more  com- 
mon than  is  generally  supposed.  The  heart  has  not  been  subjected  to 
microscopical  examination  by  any  means  so  frequently  as  the  liver 
and  the  kidneys.  The  condition  which  is  described  as  brown  atrophy 
of  heart-muscle  is  so  very  common  and  is  so  universally  considered  in 
pathological  treatises  as  one  of  the  well-recognized  forms  of  cardiac 
degeneration  as  to  make  it  desirable  that  it  should  be  as  well  under- 
stood as  possible.  So  far  as  my  own  experience  goes,  in  the  micro- 
scopical examination  of  the  heart  there  is  always  more  or  less  of  this 
so-called  brown  atrophy  existing  in  the  hearts  of  those  who  have 
reached  adult  life.  If  this  observation  be  correct,  it  would  seem  to 
indicate  that  the  condition  may  be  one  not  always  to  be  classified  as 
a  disease.  There  are  differences  between  young  and  old  hearts  which 
are  in  their  extremes  of  development  as  striking  as  the  differences 
between  health  and  disease.  Brown  atrophy  is  described  by  Ziegler, 
whose  text-book  on  pathology  is  standard,  as  a  condition  in  which  the 
"  fibres  are  smaller  than  normal  and  contain  to  a  greater  degree  than 
usual  small  yellow  pigment  granules.  These  lie  mostly  at  the  poles 
of  the  nuclei,  but  are  also  scattered  in  the  protoplasm  of  the  cells." 
It  is  noticeable  that  Ziegler  says  the  pigment  granules  are  present  to 
a  greater  degree  than  usual,  which  is  as  if  he  believes  their  presence 
to  be  normal.  My  own  belief  has  been  stated  that,  as  the  pigment 
is  invariably  present  in  adult  hearts,  some  other  explanation  of  its 
existence  must  be  found  than  the  assumption  that  it  is  always  the 
result  of  disease. 

Whether  or  not  the  nerves  of  the  heart  are  commonly  diseased, 
and  what  influence,  if  any,  their  condition  has  in  the  production  of 
recognized  complaints,  are  important  questions  which  have  occupied 
some  attention.  Nervous  tissue  is  always  difficult  to  study,  as  it  is  of 
very  delicate  structure,  and  for  this  reason,  and  because  it  has  not  yet 
been  exhaustively  examined,  no  very  satisfactory  conclusions  are  at 
present  attainable.  In  no  one  of  my  sections  from  eighty-nine  hearts 
is  there  included  any  portion  of  a  ganglion  or  a  single  medullated 


8o  THE   ORIGIN   OF   DISEASE. 

nerve  fibre,  while  on  the  other  hand  there  is  hardly  a  section  that  does 
not  include  one  or  more  non-medullated  fibres.  In  the  sections  of  the 
anterior  portion  of  the  heart,  including  the  pericardium  and  the  layer 
of  fat,  it  is  rare  to  find  one  that  contains  a  blood-vessel  without  one 
or  more  nerve  filaments.  The  nerves,  as  elsewhere,  accompany  the 
vessels,  but  these  nerves  are,  so  far  as  my  experience  goes,  all  of  the 
non-medullated  form.  The  structure  of  non-medullated  nerves  is  so 
lacking  in  distinctive  character  that  it  is  difficult  to  feel  sure  that  any 
particular  one  is  diseased  or  healthy.  In  appearance  they  are  like 
bits  of  fibrous  tissue,  and  it  is  impossible  to  decide  that  some  slightly 
unusual  appearance  is  not  due  to  a  fault  in  the  preparation  of  the 
section.  However,  there  are  in  my  possession  sections  which  have 
seemed  to  me  to  demonstrate  disease  of  the  nerves. 

The  condition  called  fragmentation,  which  has  been  described  by 
more  than  one  author,*  and  which  consists  in  a  separation  of  the  mus- 
cular fibres  transversely,  is  very  common  among  persons  who  have 
died  of  heart  disease.  It  has  been  supposed  to  be  a  giving  way  of  the 
cement  substance,  and  has  been  said  by  some  to  occur  only  in  the 
death-agony.  Neither  of  these  views  seems  to  be  very  well  sup- 
ported, and  the  likelihood  is  that  fragmentation  is  a  disease,  but  a 
true  understanding  of  its  origin  and  possible  importance  is  as  yet 
beyond  our  reach. 

In  order  to  grasp  all  that  can  be  understood  of  heart  disease,  it  is 
necessary  to  have  as  complete  a  knowledge  as  possible  of  the  anatomy 
of  the  heart.  The  description,  therefore,  that  has  been  given  of  the 
relations  of  the  cardiac  blood-vessels  to  one  another  and  to  the  mus- 
cular tissue  is  important.  There  are  at  least  two  conditions  in  this 
connection  which  are  peculiar.  These  are,  first,  that  almost  all  the 
efferent  vessels  in  the  substance  of  the  heart,  even  when  they  are 
of  good  size  and  are  accompanying  vessels  to  arterioles  having  three 
coats,  are  thin-walled  and  structurally  identical  with  the  smallest 
capillaries.  There  are,  therefore,  but  few  of  the  ordinary  veins  with 
three  coats  in  the  substance  of  the  heart.  The  second  anatomical 
peculiarity  of  importance  is  that  the  capillaries  penetrate  the  muscular 
fibres,  and  do  not  simply  ramify  among  them  and  surround  them,  as 
has  been  heretofore  believed.  It  is  difficult  to  refrain  from  specula- 
tion in  regard  to  the  effects  of  these  two  strange  anatomical  condi- 


*  Ueber  die  Fragmentation  des  Myocardium,  Alessandro  Tedeschi,  Virchow's  Archiv, 
[892,  Bd.  cxxviii.  Ss.  185-204. 


THE   HEART.  81 

tions  which  belong  to  the  heart  alone.  It  is  not  speculation,  how- 
ever, to  say  that  the  large  efferent  vessels  which  take  the  place  of 
the  small-sized  veins  which  exist  in  other  tissues  must  serve  at  least 
two  purposes  more  than  those  of  ordinary  veins  :  they  act  as  reservoirs 
to  a  greater  extent  than  common  veins,  and  they  partake  directly  in 
the  nutrition  of  the  tissue.  In  all  parts  of  the  body  the  venae  comites 
are  found  after  death  to  be  larger  than  their  companion  arteries,  but 
in  the  substance  of  the  heart  this  peculiarity  is  greatly  exaggerate'd. 
The  efferent  vessels,  which  might  well  be  named  venous  capillaries, 
are  many  times  larger  than  the  arterioles  by  which  they  are  accom- 
panied, and  therefore  their  capacity  to  serve  as  reservoirs  must  be 
vastly  greater  than  that  of  ordinary  veins,  both  because  of  their  ex- 
ceptionally great  size,  and  because  their  thin  walls  can  dilate  much 
more,  and  more  easily,  than  the  thicker  and  comparatively  rigid  walls 
of  common  veins.  It  has  been  demonstrated  by  physiologists  that 
the  capillaries  directly  nourish  the  tissues  by  the  transudation  of 
blood-corpuscles  through  their  walls  and  by  osmosis  of  the  fluid 
nutritious  portion  of  the  blood.  The  large  efferent  capillaries  which 
in  the  heart  replace  the  veins  of  other  tissues  are  structurally  identical 
with  ordinary  capillaries,  and  must  therefore  possess  the  same  power 
to  permit  of  transudation.  As  it  is  not  conceivable  that  all  the  nu- 
tritious material  has  been  abstracted  from  the  blood  before  it  reaches 
the  venous  capillaries,  they  must  to  some  extent  continue  the  function 
of  nutrition,  although  it  is  principally  performed  by  the  ordinary  capil- 
laries. Besides  their  office  of  nutrition,  blood-vessels  effect  the  work 
of  the  removal  of  the  waste  products  from  the  tissues.  In  the  heart 
it  would  seem  that  the  large  venous  capillaries,  occupying  the  place 
ordinarily  taken  by  veins,  must  afford  the  opportunity  for  waste  mate- 
rial to  enter  the  blood  with  greater  ease  and  more  completely  than  if 
there  were  veins  as  in  other  tissues.  For  veins,  being  relatively  thick- 
walled,  are  supposed  not  to  permit  transudation. 

No  illustrations  of  valve-lesions,  nor  any  extended  discussion  of 
valvular  disease  of  the  heart,  have  been  included  in  this  chapter,  be- 
cause the  subject  has  been  so  exhaustively  studied  that  it  would  not 
be  possible  to  add  much  to  what  is  known.  The  accumulation  of 
facts  in  regard  to  the  various  distortions  of  the  valves  and  the  enlarge- 
ment or  contraction  of  the  valve-openings  which  almost  invariably 
accompanies  the  changes  of  the  flaps  is  enormous. 

Although  the  physical  alterations  of  the  heart-valves  which  are 
caused  by  disease  are  so  well  known,  the  effects  of  such  changes  are 


82  THE   ORIGIN   OF   DISEASE. 

not  generally  understood.  It  is  almost  certain  that  theory  has  run 
far  beyond  what  is  warranted  by  the  facts,  and  that  the  laws  of  hydro- 
dynamics have  been  forced  into  use  in  such  a  way  as  to  lead  to  false 
deductions.  Owing  to  the  conditions  of  living  beings,  it  has  been 
impossible  as  yet  to  measure  the  various  forces  that  govern  the  heart's 
action  so  as  to  make  a  comparison  with  the  pumps  made  by  men's 
hands.  These  work  according  to  the  laws  of  water-  or  steam-pressure, 
the  size  and  strength  of  pipes,  the  action  of  mechanical  valves,  and 
other  such  things  which  can  all  be  easily  calculated  to  a  nicety  by  an 
expert  and  the  resultant  effects  predicted.  An  extended  discussion  of 
this  subject  belongs  more  properly  to  a  subsequent  part  of  this 
chapter  (page  84),  where  it  will  be  considered  in  connection  with  the 
characteristics  of  hypertrophy  of  the  heart. 

Fatty  infiltration  of  the  heart  has  commonly  been  considered  to  be 
rather  a  harmless  condition.  My  illustrations  show  that  such  is  not 
the  case,  for,  in  addition  to  the  embarrassment  of  free  movement  which 
the  presence  of  the  fat  necessarily  entails,  its  growth  takes  place  par- 
tially, at  least,  at  the  expense  of  the  muscle.  Sufficient  evidence  has 
not  been  collected  to  justify  the  positive  assertion  that  the  accumula- 
tion of  fat  upon  the  heart,  when  it  becomes  more  than  the  thin  layer 
that  is  usually  found  upon  the  hearts  of  all  but  very  young  persons, 
is  necessarily  a  disease.  When  the  layer  of  fat  does  become  thick,  the 
amount  of  muscle  is  sometimes  proportionately  diminished  (Fig.  46), 
and,  although  it  would  be  unwarrantable  to  say  that  this  is  invariably 
the  case,  the  mode  of  growth  of  the  fat  makes  it  in  the  highest  degree 
probable  that  a  thick  fat  layer  always  morbidly  interferes  with  the 
integrity  of  the  muscle.  Its  very  presence  is  obstructive,  and  its  habit 
is  to  force  itself  into  the  cardiac  septa  and  between  the  muscular 
fibres,  in  doing  which  it  always  destroys  some  of  them.  Besides 
this,  the  fat  itself  is  frequently  the  seat  of  disease.  Inflammation  of 
the  heart-fat  and  its  condensation  and  conversion  into  morbid  fibroid 
tissue  are  of  frequent  occurrence.  This  has  been  discussed  and  the 
appearances  illustrated,  and  it  need  not,  therefore,  be  repeated.  It  is 
sufficient  to  direct  attention  again  to  the  facts  that  the  fat  seems  to  be 
an  especially  vulnerable  portion  of  the  heart,  and  that  disease  is  even 
more  prone  to  arise  upon  the  surface  of  the  heart  than  in  the  deeper 
portions.  This  peculiarity  it  has  in  common  with  most  of  the  other 
great  organs,  as  will  be  shown  when  the  consideration  of  their  morbid 
lesions  is  reached. 

It  would  be  difficult  to  exaggerate  the  importance  of  fibroid  de- 


THE   HEART.  83 

generation  of  the  heart.  Some  degree  of  it  is  a  necessary  accom- 
paniment of  extreme  old  age ;  and,  on  the  other  hand,  no  period  of 
life  seems  too  early  for  it  to  show  itself  if  the  requisite  conditions 
arise.  Fibrosis  in  the  heart  necessarily  interferes  with  the  efficient 
performance  of  its  function,  for  the  morbid  fibroid  tissue  always  re- 
places muscular  tissue  if  it  is  not  partially  formed  by  an  actual  con- 
version of  muscle.  Some  of  these  peculiarities  are  graphically  demon- 
strated by  the  illustrations. 

Hollowing  and  unnatural  tenuity  of  the  muscular  fibres  are  forms 
of  degeneration  of  the  heart  which  are  very  common.  The  impor- 
tance of  degeneration  of  the  cardiac  walls  has  not  been  heretofore 
underestimated,  for  no  one  has  bestowed  thought  upon  the  subject 
without  appreciating  that  anything  which  weakens  the  heart-muscle 
strikes  a  blow  at  the  very  root  of  its  power. 

Although  many  writings  upon  heart  disease  are  pervaded  by  a  tone 
which  shows  that  the  authors  were  impressed  with  the  great  impor- 
tance of  degeneration  of  the  cardiac  walls,  the  subject  has  not  been 
formulated,  and  as  yet  but  few  well-established  facts  in  connection 
with  it  have  been  collected.  The  number  of  hearts  microscopically 
examined  by  me  has  been  sufficiently  great  to  warrant  the  asser- 
tion that  morbid  hollowing  of  the  muscular  fibres  is  an  exceedingly 
common  lesion.  The  disease  has  been  recognized  for  some  time,  and 
is  generally  called  vacuolation  and  attributed  to  hyaloid  degeneration. 
It  is  very  destructive  of  the  muscle  if  it  attains  any  great  degree  of 
development.  This  is  conclusively  proved  by  the  illustrations,  which 
show  fibres  so  completely  excavated  as  to  convert  them  into  thin- 
walled  tubes.  It  is  not  possible  as  yet  to  know  its  origin,  nor  to 
watch  all  the  various  steps  of  this  singular  disease.  Certain  facts, 
however,  have  been  ascertained.  The  pigment  which  in  elderly  per- 
sons is  always  present  to  some  extent  in  the  fibres  lying  adjacent  to 
the  poles  of  their  nuclei,  and  the  fact,  to  which  I  have  directed  atten- 
tion, that  the  capillaries  penetrate  the  muscular  fibres,  must  have  an 
important  bearing  on  the  process  of  hollowing,  for  the  part  of  the 
fibres  that  becomes  hollow  is  that  ordinarily  occupied  by  the  pigment 
and  through  which  the  capillaries  pass.  It  was  said  in  the  earlier 
portion  of  this  chapter  that  the  most  probable  explanation  of  the 
hollowing  of  the  fibres  is  that  it  is  a  cystic  degeneration,  the  hollow 
portions  of  the  fibres  being  minute  cysts  which  originated  in  the 
capillaries, — that  the  hollow  spaces,  therefore,  are  capillary  aneurisms. 
This  is  only  a  theory,  for  evidence  has  not  been  collected  sufficient  to 


84  THE   ORIGIN   OF   DISEASE. 

prove  it  a  fact,  but  the  more  one  considers  the  anatomical  relations  of 
the  fibres  with  the  blood-vessels  the  more  probable  does  it  seem  that 
such  is  the  correct  explanation.  The  pigment  at  the  poles  of  the 
nuclei  is  so  much  like  altered  blood  which  has  exuded  from  the 
vessels,  as  blood  is  found  in  other  parts  of  the  body  in  states  of  dis- 
ease, that  it  is  impossible  to  avoid  the  thought  that  it  may  have 
some  relation  with  the  blood.  As  yet  we  know  nothing  of  the  origin 
and  meaning  of  the  pigment.  Perhaps  further  study  of  the  develop- 
ment of  muscular  tissue  in  human  and  other  mammalian  embryos 
will  some  day  lead  to  a  complete  explanation.  The  occurrence  of 
cystic  disease  of  the  heart,  which  has  been  fully  established  (page 
75),  is  a  curious  and  interesting  phenomenon.  Cysts  in  the  heart  are 
probably  very  rare. 

The  most  important  conclusion  I  have  reached  is  that  "  compensa- 
tory hypertrophy  of  the  heart,"  as  it  is  ordinarily  described  and  under- 
stood, has  no  existence.  All  hypertrophied  hearts  are  degenerated  and 
weakened.  This  position  will  be  very  difficult  to  establish,  because  of 
the  prejudice  that  exists  in  favor  of  old  beliefs  to  the  contrary  which 
have  been  so  long  accepted.  If  it  were  possible  to  divest  the  mind 
of  preconceived  opinions  and  thus  approach  the  subject  entirely  un- 
biassed, it  would  be  much  less  difficult  to  reach  a  just  conclusion. 
When  auscultation  began  to  be  practised  and  cardiac  murmurs  were 
heard,  it  was  soon  discovered  that  their  existence  almost  certainly 
indicated  distortion  of  the  valves.  The  obviousness  of  the  murmurs, 
which  if  loud  can  be  distinguished  by  a  tyro,  and  the  discovery  of 
their  connection  with  changes  of  the  valves,  soon  gave  rise  to  an  exag- 
gerated estimate  of  the  importance  of  valvular  disease.  The  minds 
of  students  of  heart  disease  were  occupied  with  the  valves  almost  to 
the  exclusion  of  other  forms  of  disease.  Every  affection  of  the  heart 
was  made  to  centre  in  the  valves  and  was  explained  as  having  origi- 
nated from  valvular  disease.  More  lately  it  has  been  learned  that 
valvular  disease  may  be  by  no  means  so  dangerous  as  was  formerly 
supposed,  and  it  is  now  well  established  that  valvular  distortions  of 
such  a  character  as  to  produce  loud  murmurs  may  exist  in  youth  and 
yet  the  individuals  live  in  good  health  to  old  age.  The  consideration 
of  such  cases  ought  to  have  induced  a  fuller  realization  of  the  fallacy 
of  the  use,  or  rather  misuse,  that  has  been  made  of  the  laws  of  hydro- 
dynamics. It  has  been  taught  and  almost  universally  accepted  that 
regurgitation,  which  throws  extra  work  upon  the  walls  of  the  cavity 
of  the  heart  which  is  behind  the  leaking  valve,  is  invariably  answered 


THE   HEART.  85 

by  nature  by  an  increase  of  muscle,  that  the  walls  of  the  cavity  thicken 
and  grow  in  strength,  that  hypertrophy  results,  and  that  it  is  compen- 
satory. It  is  my  belief,  founded  on  observation,  that  regurgitation 
does  not  always  cause  hypertrophy.  If  this  can  be  shown  to  be  true, 
the  theories  in  regard  to  compensation  become  untenable.  The  doc- 
trine that  muscles  increase  when  called  on  to  perform  severe  labor 
has  been  pushed  much  further  than  is  justified  by  the  facts.  The 
truth  is,  muscles  improve  in  efficiency  much  more  than  they  increase 
in  bulk  and  weight.  Exercise  develops  the  muscles  of  a  man  in  good 
health  so  that  it  becomes  possible  for  him  to  perform  feats  of  strength 
which  would  have  been  impossible  without  the  requisite  preparation ; 
but  this  quality  is  restricted  within  narrow  limits,  and  the  actual  in- 
crease of  the  muscles  when  exercised  is  not  great,  while  the  individual 
frequently  loses  weight.  Few  men  can  become  superior  athletes,  and 
if  it  is  attempted  to  make  one  of  a  person  unfitted  for  it  he  rapidly 
becomes  "  stale"  and  deteriorates.  No  development  of  the  muscles 
of  an  athlete  trained  for  contest,  or  of  any  special  set  of  muscles  like 
those  of  the  arm  of  a  blacksmith  or  of  the  upper  arm  of  a  file-striker, 
is  comparable  to  the  increase  in  size  and  weight  of  the  heart  in  hyper- 
trophy which  is  said  to  be  compensatory  and  conservative  !  Nor  is 
any  allowance  made  for  the  fact  that  hypertrophy  of  the  heart  occurs 
only  in  the  diseased.  Upon  general  principles  it  seems  unlikely  that 
the  heart  can  in  disease  increase  so  wonderfully  in  size  and  strength 
to  compensate  for  the  harm  done  by  such  a  defect  as  a  leak,  when  the 
most  healthy  men,  even  if  every  opportunity  is  given  them  and  there 
is  no  disease  to  interfere,  can  increase  the  bulk  of  their  muscles  so  very 
little,  and  when,  besides  this,  even  among  those  carefully  selected,  men 
often  fail  under  training  and  the  muscles  dwindle.  It  has  never  been 
demonstrated  that  the  hypertrophied  heart  pumps  with  increased  force, 
or  that  the  pressure  within  the  arteries  is  raised.  Such  a  demonstra- 
tion could  be  made  only  by  the  introduction  into  an  artery  of  an  instru- 
ment of  precision  to  measure  the  blood-pressure ;  and  circumstances 
render  this  inadmissible.  That  the  arterial  blood-pressure  is  increased 
when  the  heart  is  hypertrophied  is  inferred  because  the  cardiac  im- 
pulse becomes  heaving  and  forcible,  and  because  the  pulse  when  felt 
with  the  finger  imparts  a  sensation  as  of  fulness  and  has  a  bounding 
character.  The  question  is  not  asked  how  much  of  the  heaving 
motion  is  due  to  increase  of  size  of  the  organ  which  has  become  too 
big  for  the  chest.  Nor  is  it  asked  if  the  impression  of  "  high-tension 
pulse"  may  be  due  to  thickening  and  change  of  character  of  the 


86  THE   ORIGIN   OF   DISEASE. 

arterial  walls.  Whatever  may  be  thought  of  that  which  has  been 
alleged  in  support  of  the  opinion  that  compensatory  hypertrophy  of 
the  heart  does  not  exist,  there  is  another  and  a  more  objective  side 
from  which  the  question  may  be  approached, — the  investigation  of 
the  actual  physical  condition  of  enlarged  hearts.  Both  the  gross  and 
the  microscopical  appearances  of  hypertrophied  hearts  show  that  the 
muscular  tissue  is  always  diseased.  It  is  almost  certain  that  in  hyper- 
trophied hearts  the  number  of  muscular  fibres  is  increased,  and  this 
has  for  a  long  time  been  the  opinion  of  pathologists.*  From  this  fact 
it  has  been  argued  that  the  heart  must  be  strong,  and  without  further 
consideration  of  the  many  complicating  circumstances  the  compen- 
satory character  of  cardiac  enlargement  was  assumed.  Compensatory 
hypertrophy  is  a  convenient  and  attractive  theoretical  possibility,  and 
it  is  probable  that  if  a  healthy  athlete  were  killed  when  in  the  perfec- 
tion of  training,  his  heart  would  be  found  to  be  slightly  larger  and 
heavier  than  before  the  training  was  begun ;  its  condition  of  pliability 
and  muscular  tissue  would  be  perfect ;  but  it  is  not  conceivable  that  the 
healthy  heart  of  an  athlete  could  attain  the  size  of  the  hypertrophied 
hearts  of  diseased  persons,  or  could  in  the  most  distant  way  resemble 
the  deformed  organ  called  the  cor  bovinum.  In  every  respect  the  ap- 
pearance of  the  hypertrophied  heart  contradicts  the  assumption  of 
increased  strength.  The  walls,  though  thick,  are  generally  hard  and 
stiff,  and  the  heart  has  lost  its  pliability  to  such  an  extent  that  the 
cavities  stand  open.  It  is  most  improbable  that  it  is  able  in  such  a 
condition  to  empty  itself  of  blood.  The  contractions  are  inefficient 
squeezes  that  expel  only  a  small  portion  of  the  blood  from  the  cavities, 
instead  of  the  nearly  complete  closures  that  take  place  in  the  healthy 
condition.  The  muscle  is  of  unnatural  color  and  is  easily  torn.  Thick 
cardiac  walls,  enlarged  cavities,  and  very  soft  muscular  substance  are 
the  features  of  another  common  form  of  heart  disease.  Such  a  heart 
tears  easily,  and  when  removed  from  the  body  falls  into  an  almost 
shapeless  mass,  so  that  it  is  hard  to  distinguish  its  natural  form. 
This  is  not  suggestive  of  unnaturally  great  strength,  although  the 
heart  may  be  of  greatly  increased  size  and  weight.  When  a  piece  of 
the  thick  and  heavy  wall  of  an  hypertrophied  heart  is  subjected  to 
microscopical  examination,  it  is  never  found  healthy.  It  is  unneces- 
sary to  repeat  in  detail  what  has  already  been  said  in  regard  to  the 


*  Pathological  Anatomy,  by  Samuel  Wilks  and  Walter  Moxon,  Lindsay  &  Blakiston, 
Philadelphia,  1875,  p.  113. 


THE   HEART.  87 

various  minute  changes  of  the  cardiac  muscle.  At  least  one  of  the 
forms  of  degeneration  is  certain  to  be  found  in  enlarged  hearts.  Car- 
diac hypertrophy  is  not  the  result  of  an  increase  in  the  amount  of 
healthy  muscle  as  nature's  answer  to  the  extra  work  caused  by  re- 
gurgitation  through  a  leaky  valve,  but  of  degeneration  of  the  muscle. 
There  is  no  evidence  that  the  valvulitis  and  leaking  which  so  often 
result  from  endocarditis  precede  the  disease  of  the  muscular  tissue 
which  is  their  invariable  companion,  and  it  is  well  known  that  in 
many  cases  the  walls  become  diseased  and  the  heart  enormously 
hypertrophied  and  yet  all  the  valves  remain  perfectly  sound.  Of  the 
truth  of  the  statements  made  in  regard  to  the  origin  of  hypertrophy 
of  the  heart  there  should  be  no  doubt  in  the  mind  of  any  one  expe- 
rienced in  its  study;  and  if  once  it  is  acknowledged  that  the  en- 
larged heart  is  always  degenerated  and  weakened,  there  is  no  escape 
from  accepting  my  view  that  "  compensatory  hypertrophy"  has  no 
existence. 


CHAPTER    VI. 

THE    LUNGS. 

OF  all  the  organs  the  lungs  are  the  most  delicate  and  most  liable  to 
disease.  This  is  probably  because  the  air  has  free  access  to  their  inner 
surface,  and  they  are  therefore  subjected  to  rougher  usage  than  the 
other  great  organs,  which  are  buried  deep  in  the  body  and  protected 
from  ordinary  external  irritants.  The  air  is  subject  to  great  variation 
in  the  degree  of  its  moisture  and  its  temperature,  and  it  often  carries  in 
it  irritant  or  poisonous  material.  The  lungs  are  affected  by  all  these 
changing  conditions  of  the  air  in  a  manner  that  has  no  parallel  in  the 
other  organs.  Even  the  intestinal  canal,  which  has  direct  communi- 
cation with  the  air,  is  so  arranged  that  but  little  air  ever  gets  into  it. 
The  lungs,  like  any  other  part  of  the  organism,  are  liable  to  sudden 
attacks  of  acute  disease,  but  in  the  lungs  perhaps  more  frequently 
than  in  other  organs  there  will  be  found  some  antecedent  chronic 
disease  which  paved  the  way  and  rendered  them  liable  to  the  acute 
attack.  At  very  early  periods  of  life,  as  will  be  presently  shown, 
processes  of  degeneration  are  common  which  are  parallel  in  every 
respect  with  those  which  occur  in  persons  of  more  advanced  years. 
Such  changes  are  often  of  slight  extent  and  may  readily  be  over- 
looked, but  they  are  none  the  less  important.  Emphysema  and 
fibrosis  and  vascular  disease  are,  so  far  as  is  at  present  known,  the 
common  forms  of  chronic  pulmonary  decay.  A  matter  of  great 
importance,  and  one  which  must  never  be  lost  sight  of,  is  the  latent 
manner  in  which  these  degenerations  progress.  Extensive  emphy- 
sema and  fibrosis  or  vascular  disease  may  often  be  found  in  the  bodies 
of  persons  who  had  suffered  no  attack  of  sickness  while  these  de- 
generative conditions  had  been  progressing,  but  had  enjoyed  suffi- 
ciently good  health  to  be  able  unimpeded  to  pursue  their  ordinary 
vocations.  It  has  already  been  pointed  out  that  there  are  recog- 
nizable physical  differences  of  appearance  between  the  hearts  of  the 
young  and  those  of  the  old.  The  same  is  true  of  the  lung.  As  life 
progresses,  the  amount  of  fibrous  tissue  in  the  lung  increases  and 
the  actual  number  of  the  air-vesicles  becomes  less,  and  at  the  same 
time  the  supply  of  capillaries  to  the  walls  of  the  air-sacs  becomes  less 
88 


THE   LUNGS.  89 

abundant  and  less  efficient.  All  this  is  true,  but  it  is  very  difficult 
to  make  an  ocular  demonstration  of  it.  Emphysema  and  fibrosis  as 
names  of  diseases  are  terms  which  are  useful  and  probably  necessary 
to  describe  physical  conditions  which  are  easily  recognized  by  the  un- 
aided eye.  In  descriptions  of  them  in  text-books  allusion  is  usually 
made  to  diseased  conditions  of  the  blood-vessels  as  common  accom- 
paniments. The  likelihood,  however,  is  that  these  two  widely  different- 
looking  conditions  are  the  same  disease,  or  only  the  varying  results 
of  a  single  cause  which  underlies  them.  They  are  not  more  unlike 
each  other  than  are  scirrhus  and  some  of  the  forms  of  soft  fungous 
cancer,  and  yet  no  one  doubts  that  both  of  these  are  properly  classi- 
fied as  one  disease.  Emphysema  has  commonly  been  described  as 
secondary  to  some  other  disease,  but  too  much  emphasis  has  been 
placed  upon  the  presence  of  obstruction  of  the  bronchial  outlets  from 
the  air-sacs  and  consequent  enlargement  of  them  by  internal  me- 
chanical pressure  as  an  absolute  necessity  to  the  production  of  emphy- 
sematous  dilatation.  There  is  no  good  reason  for  supposing  that 
mechanical  obstruction  is  a  necessary  feature  in  the  production  of 
emphysema;  on  the  contrary,  it  is  likely  that  it  arises  as  a  result  of 
pure  fibrosis  and  degeneration.  The  possibility  of  the  existence  of 
acute  vesicular  emphysema  without  change  of  structure  of  the  alveolar 
walls  may  well  be  doubted.  For  all  practical  purposes,  at  any  rate, 
such  a  disease  does  not  exist,  for,  even  supposing  that  there  was  a 
mechanical  obstruction  to  the  bronchial  outlet  of  a  portion  of  the 
lung,  with  resultant  dilatation,  the  dilatation  could  hardly  have  begun 
before  the  tissues  would  suffer  from  the  stretching  so  that  structural 
change  would  result. 

Fibrosis  of  the  lung  is  generally  classified  and  described  in  con- 
nection with  phthisis  pulmonalis  or  as  a  form  of  pneumonia  rather 
than  with  emphysema  or  as  a  degenerative  condition.  From  the  stand- 
point of  the  clinician  fibroid  phthisis  has  such  positive  individuality 
that  many  of  the  most  enthusiastic  advocates  of  the  theory  that  con- 
sumption of  the  lungs  cannot  exist  without  the  bacillus  tuberculosis 
as  its  original  cause  have  been  forced  to  admit  that  the  fibroid  form  of 
consumption  may  have  an  independent  existence.  Pulmonary  fibrosis 
is  also  described  as  a  consequence  of  broncho-pneumonia  and  of  the 
process  called  pleurogenous  interlobular  pneumonia.  In  addition, 
however,  to  these  conditions,  which  are  perfectly  well  recognized 
clinical  entities  with  definite  pathological  lesions,  there  will  often  be 
found  in  the  bodies  of  persons  dead  of  chronic  disease,  and  especially 


90  THE   ORIGIN   OF   DISEASE. 

in  those  with  emphysema,  an  increase  of  fibrous  tissue  in  the  lungs, 
which,  although  not  always  of  great  extent,  is  as  easy  to  recognize  as 
are  coarser  lesions.  Emphysema  and  fibrosis  of  the  lungs  are  in  their 
full  development  as  unlike  as  any  two  processes  could  well  be,  and 
yet  the  evidence  in  favor  of  their  intimate  association  if  not  of  their 
common  origin  is  overwhelming.  Vascular  disease  must  be  looked 
upon  as  an  essential  part  of  both,  for  it  is  always  associated  with  them 
to  a  greater  or  less  extent. 

The  cause  is  at  present  obscure.  Fibrosis,  emphysema,  and  vas- 
cular changes  are  necessary  accompaniments  of  age  if  life  be  suffi- 
ciently prolonged,  and  they  may  reach  extreme  forms  of  development 
without  the  individual  having  had  any  external  manifestation  of 
them.  Their  progress  may  be  absolutely  latent,  although  the  indi- 
vidual usually  presents  the  ordinary  appearances  of  growing  older. 
On  the  other  hand,  the  influence  of  attacks  of  inflammation  of  the 
respiratory  apparatus  in  producing  emphysema,  fibrosis,  and  vas- 
cular disease  is  beyond  question  very  great,  whether  the  inflamma- 
tion be  in  the  form  of  pleurisy,  pneumonia,  or  bronchitis.  The 
lungs  are  capable  at  every  period  of  life  and  in  each  individual  of 
becoming  acutely  diseased  if  subjected  to  a  sufficient  degree  of  irri- 
tation. The  irritant  which  is  the  most  prolific  cause  of  such  disease 
is  the  atmosphere,  which  is  liable  at  all  times  to  extreme  changes, 
but  especially  in  spring,  when  the  weather  is  most  variable  and  the 
temperature  subject  to  the  greatest  extremes.  While  it  is  true  that 
entirely  healthy  lungs  may  become  acutely  inflamed  if  subjected  to 
sufficient  irritation,  it  is  important  to  remember  that  lungs  which  have 
been  rendered  imperfect  by  degeneration  or  a  previous  acute  attack 
will  succumb  to  an  irritation  that  would  have  no  effect  upon  healthy 
lungs.  The  two  conditions  acute  inflammation  and  chronic  latent 
degeneration  act  and  react  one  upon  the  other  in  such  a  manner  that 
it  is  often  impossible  in  a  given  case  to  ascertain  which  of  the  two 
was  the  original  offender.  That  chronic  latent  degeneration  may 
originate  spontaneously  does  not  admit  of  doubt,  and  it  is  equally 
certain  that  an  attack  of  acute  inflammation  of  the  lungs  may  leave 
them  slightly  injured,  if  it  does  not  always  leave  them  more  or  less 
imperfect.  Such  an  imperfection,  produced  by  acute  inflammation, 
may  be  so  slight  as  never  to  do  any  harm ;  it  may  lie  dormant  to 
furnish  the  basis  of  origin  for  subsequent  inflammatory  attacks,  or  it 
may  progress  after  the  recovery  from  the  original  acute  attack  as 
a  latent  degeneration,  which  will  go  on  to  a  high  degree  of  develop- 


FIG.  63. — PULMONARY  EMPHYSEMA.     (X  7.) 

Lung  of  a  man  thirty-one  years  of  age  who  died  of  Bright 's  disease.  The  portion 
included  is  everywhere  covered  with  pleura  except  at  the  bottom,  which  is  a  cut  surface. 
On  the  right,  below  the  middle,  is  an  emphysematous  patch,  in  which  most  of  the  alveoli 
have  disappeared,  and  there  remain  only  thin  and  delicate  broken  fibrous  strands.  These 
strands  are  entirely  without  blood-supply,  and  were  therefore  unable  to  subserve  their 
natural  function  of  aerating  the  blood.  The  fibrous  tissue  surrounding  the  emphysematous 
patch  is  very  heavy,  and  below  is  a  deep  sulcus  :  this  it  is  which  makes  patches  of  emphy- 
sema appear  as  blebs  upon  the  lung  surface.  Upon  the  left  side  and  at  the  top  are  other 
emphysematous  areas,  but  they  are  not  so  sharply  separated  from  the  more  nearly  healthy 
regions  as  is  the  bleb  on  the  right. 


FIG.  63. 


1  mm. 


FIG.  64. — PULMONARY  EMPHYSEMA.     (X  7-) 

From  a  man  aged  twenty-nine  years  who  died  of  Bright' s  disease  and  peritonitis.  The 
edge  below  and  to  the  left  is  a  cut  surface,  the  rest  is  covered  by  pleura.  Above  are  two 
emphysematous  blebs,  one  to  the  right  and  one  to  the  left  of  a  fibrous  band  which  runs  to 
the  top  of  the  section.  In  the  patch  to  the  right  the  alveoli  are  exceedingly  broken,  but 
few  circles  remaining,  and  the  fibrous  lines  are  thin  and  the  spaces  large,  several  air-sacs 
having  broken  into  one.  Below  are  heavy  bands  of  fibrous  material,  containing  blood- 
vessels and  bronchi. 

FIG.  65. — PULMONARY  EMPHYSEMA  IN  A  YOUNG  INFANT.     (X  6.) 

Lung  of  an  infant  six  weeks  old  that  died  suddenly.  The  picture  is  to  show  the  bleb. 
Its  wall  is  thin  and  fibrous  and  without  blood-supply  upon  the  free  side.  Next  the  lung  it 
is  much  thicker,  and  resembles  the  fibrous  wall  of  a  cyst.  The  bleb  was  unbroken  at  the 
post-mortem  examination,  and  was  full  of  air  which  seemed  imprisoned,  there  having  been 
no  channel  for  its  escape.  The  curious  shape  of  the  line  and  the  breaks  in  it  resulted 
from  imperfect  cutting  and  the  way  in  which  the  walls  were  folded  in  course  of  prepara- 
tion. In  portions  of  the  lung  substance  the  openings  are  so  large  that  it  seems  that  they 
too  must  be  emphysematous.  The  bottom  of  the  picture  shows  a  cut  surface  ;  the  other 
sides  are  covered  by  pleura. 


FIG.  64. 


i  nun 


FIG.  65. 


THE   LUNGS.  91 

ment  without  any  external  manifestation  in  the  form  of  an  attack  of 
sickness  or  even  of  incapacitating  physical  weakness. 

The  illustrations  exhibit  a  number  of  the  peculiarities  of  disease  of 
the  lungs.  Fig.  63  represents  under  low  amplification  a  section  of  the 
lung  of  a  man  thirty-one  years  of  age  who  died  of  Bright's  disease. 
It  makes  an  excellent  showing  of  the  ordinary  appearances  of  emphy- 
sema when  it  is  fully  developed.  Upon  the  right  side  is  an  emphy- 
sematous  bleb  which  is  separated  from  the  surrounding  tissue  by  a 
thick  fibrous  layer,  and  below  is  a  deep  sulcus  which  must  have 
caused  the  emphysematous  bleb  to  stand  out  from  the  surface,  as 
it  is  common  for  emphysematous  blebs  to  do  when  the  lung  is  dis- 
tended with  air.  Within  the  patch  of  emphysema  there  are  no  healthy 
air-sacs,  but  only  irregular  and  broken  fibrous  threads.  These  threads 
when  examined  with  higher  amplification  are  seen  to  be  generally 
without  vascular  supply,  which  is  so  rich  in  the  healthy  alveolar  walls. 
The  capillaries  had  atrophied,  leaving  fibrous  tissue  which  was  so  ill 
nourished  as  to  be  unable  to  maintain  its  own  existence ;  much  less 
was  it  capable  of  taking  up  the  oxygen  of  any  air  that  might  be  in 
the  dilated  air-sacs.  Throughout  the  section  is  seen  an  alternation 
of  broken-down  air-sacs  and  increase  of  fibrous  tissue.  Such  are  the 
common  appearances  of  emphysema,  the  increase  of  the  fibrous  tissue 
and  the  destruction  of  the  vascular  supply  being  as  much  parts  of 
the  disease  as  is  the  increased  size  of  the  air-sacs  themselves.  Fig. 
64  is  from  the  emphysematous  lung  of  a  man  twenty-nine  years  old 
who  died  of  Bright's  disease,  peritonitis,  and  other  complications. 
It  shows,  as  the  previously  mentioned  drawing  does,  that  fibrosis  is 
as  much  a  part  of  emphysema  as  is  dilatation  of  the  air-sacs.  There 
are  no  healthy  air-sacs,  the  fibrous  trabeculae  are  much  heavier  than 
natural,  and  the  vessels  are  thickened;  but  this  latter  feature  of  the 
disease  could  be  satisfactorily  studied  only  by  the  use  of  greater  am- 
plification. 

Fig.  65  presents  a  strong  contrast  with  the  two  last  described 
drawings.  It  is  a  section  of  the  lung  of  a  previously  healthy  infant 
six  weeks  old  that  died  suddenly  of  convulsions.  The  baby  was  a 
mulatto  that  had  been  nursed  by  its  mother,  and  no  lesion  satisfac- 
torily explaining  the  death  was  found  at  the  post-mortem  examina- 
tion. There  were  thrombi  in  the  veins ;  in  the  kidneys  these  were 
very  large,  so  that  the  veins  were  enormously  distended,  and  in  the 
drawing  are  shown  veins  in  the  lung  containing  clots ;  but  whether 
thrombosis  is  to  be  looked  upon  as  the  cause  of  the  fatal  attack  or 


92  THE   ORIGIN   OF   DISEASE. 

only  as  one  of  its  effects  cannot  be  known.  The  drawing  presents 
two  special  points  of  interest.  In  the  first  place,  it  shows  in  a  graphic 
manner  the  great  difference  in  appearance  between  the  lung  in  early 
infancy  and  at  later  periods  of  life.  The  amplification  used  was  nearly 
the  same  for  this  and  the  two  previously  described  drawings,  and  the 
contrast  of  appearance  is  so  great  that  it  need  not  be  much  dwelt 
upon.  In  the  infant  lung  the  amount  of  solid  tissue  is  greater  and 
the  amount  of  air-space  less  relatively  than  in  the  adult  lung. 

The  second  point  of  interest  is  the  existence  of  emphysema  in  an 
infant  of  six  weeks.  The  lesion  certainly  can  be  classed  only  as  em- 
physema, for  with  the  present  understanding  of  diseases  of  the  lungs 
no  other  term  describes  such  an  enlarged  air-bleb  as  the  one  repre- 
sented. This  bleb  is  bounded  upon  its  free  side  by  a  thin  fibrous 
membrane  which  is  entirely  without  blood-supply,  while  upon  the 
side  next  the  lung  is  a  thick  layer  of  fibrous  tissue  which  is  not  richly 
supplied  with  blood. 

A  strange  phase  of  the  clinical  admixture  of  acute  and  chronic 
disease  is  illustrated  by  Fig.  66 ;  this  represents  the  lung  of  a  man 
twenty-six  years  old  who  died  of  typhoid  fever.  Most  of  the  air-sacs 
of  natural  size  which  are  included  in  the  drawing  contain  a  good 
deal  of  cellular  and  fibrinous  exudate,  and  in  other  portions  of  the 
lungs  the  alveoli  were  filled  with  blood.  This  condition  of  things  is 
almost  universal  in  the  lungs  of  persons  dead  of  typhoid  fever  at  any 
but  the  earliest  periods.  But  besides  the  exudation,  which  was  an 
acute  process,  the  illustration  shows  a  group  of  air-sacs  which  are 
much  dilated,  and  of  these  the  walls  are  fibrous  and  heavy  and  in 
places  broken,  so  that  the  number  of  vesicles  has  become  much  less 
than  when  the  same  region  was  healthy.  The  broken  condition  of 
the  alveoli  and  the  thick,  fibrous,  avascular  tissue  around  their  walls 
are  very  striking. 

Another  notable  feature  is  that  this  emphysematous  area  is  very 
much  pigmented.  Although  the  lung  tissue  is  astonishingly  tolerant 
of  the  presence  of  pigment,  and  often  such  quantities  of  it  are  present 
in  lungs  otherwise  apparently  healthy  as  to  make  them  almost  black, 
it  seems  to  me  that  pigment  is  frequently  a  source  of  disease.  It 
is  common  to  find  evidence  of  inflammation  or  degeneration  around 
pigmented  areas,  and  it  is  not  impossible  that  the  pigment  repre- 
sented in  the  illustration  was  the  cause  of  the  degeneration  that  had 
occurred.  The  emphysema,  fibrosis,  and  decreased  vascularity  must 
have  been  the  results  of  chronic  degeneration,  and  must  have  ex- 


FIG.  66. — PULMONARY  EMPHYSEMA  AND  FIBROSIS  IN  A  YOUNG  MAN  DEAD  OF  ACUTE 

DISEASE,     (x  25.) 

Section  of  lung  of  a  man  of  twenty-six  years  who  died  of  typhoid  fever.  The  upper 
curved  edge  is  covered  by  pleura  which  is  much  thickened  and  pigmented.  There  is 
general  cellular  infiltration,  most  of  the  alveoli  being  nearly  solid.  The  unusual  feature 
of  disease  is  that  there  are  large  emphysematous  cavities  with  thick  fibrous  walls  which 
are  entirely  avascular. 

FIG.  67. — FIBROID  SURFACE  OF  THE  LUNG,     (x  21.) 

From  a  man  of  fifty-seven  years  who  died  of  Bright' s  disease.  The  pleura  (/)  can  be 
distinguished  only  to  the  left  of  the  centre.  It  is  evident  that  the  fibrous  material  grew 
partly  upon  and  partly  underneath  the  pleura  ;  between  i  and  k  is  epipleural  and  between 
k  and  /  subpleural  growth.  The  subpleural  fibrous  tissue  contains  many  nuclei,  and  there 
are  blood-vessels  in  both  the  epipleural  and  subpleural  layers.  The  line  of  separation  of 
the  two  fibrous  layers  is  very  distinct,  and  at  places  along  it  there  is  much  pigmentation. 
Below  /  is  the  lung  tissue. 


FIG.  66. 


FIG.  67. 


THE   LUNGS.  93 

isted  in  the  individual  for  some  time  before  he  was  attacked  by  the 
typhoid  fever  of  which  he  died.  The  case,  therefore,  affords  evidence 
of  the  correctness  of  the  statement  that  lesions  of  chronic  disease  are 
commonly  found  in  those  who  have  died  of  acute  attacks  and  in  whom 
the  clinical  history  reveals  no  previous  illness. 

In  Fig.  67  is  represented  an  entirely  different  phase  of  fibroid  dis- 
ease. It  is  of  the  lung  of  a  man  fifty-seven  years  old  who  died  of 
Bright's  disease  after  a  prolonged  illness,  and  in  whom  there  was 
fibrosis  of  the  most  extreme  degree  in  many  organs  and  tissues,  with 
numerous  calcareous  deposits  in  many  places  in  the  body.  The 
fibrosis  shown  in  the  illustration  is  of  the  form  which  is  a  part  of 
pleurogenous  interlobular  pneumonia.  Upon  the  surface  of  the  lung 
and  occupying  the  position  of  the  pleura  is  a  thick  layer  of  fibrous 
material,  which  looks  at  first  sight  as  if  it  was  due  simply  to  pleural 
thickening.  More  careful  examination  reveals,  however,  that  it  is 
of  more  complex  origin.  The  fibrous  layer  is  seen  to  be  composed 
of  two  strata  of  different  appearances,  and  at  one  place  (see  descrip- 
tion of  figure)  the  pleura  can  be  distinguished.  The  situation  of  this 
portion  of  pleura  which  remains  shows  that  part  of  the  fibrous  tissue 
grew  upon  and  outside  of  the  pleura,  while  another  portion  grew 
below  it  and  therefore  at  the  expense  of  the  lung. 

The  epipleural  fibrous  tissue  is  thick  and  dense,  and  in  structure 
similar  to  that  of  the  fibromas  that  are  so  commonly  found  upon  the 
surface  of  the  lung  and  spleen,  while  the  subpleural  portion  is  of  a 
structure  much  less  dense.  Along  the  line  of  contact  of  the  epi- 
pleural and  subpleural  layers,  which  is  the  situation  of  the  pleura, 
there  is  much  pigmentation.  When  the  section  is  examined  with 
different  amplifications  along  the  line  of  junction  of  the  lung  with  the 
subpleural  fibrous  tissue,  it  is  plainly  seen  that  the  fibrous  tissue  grew 
at  the  expense  of  the  lung.  Alveoli  can  be  seen  with  their  walls 
thickened  and  variously  filling  up  by  the  growth  of  fibrous  tissue, 
the  porous  lung  being  converted  into  solid  fibrous  tissue.  The  loss 
of  efficiency  of  the  lung  from  such  a  degeneration  must  be  very 
great,  for,  in  addition  to  the  direct  reduction  of  the  amount  of  tissue 
capable  of  performing  its  function,  the  freedom  of  its  motions  must 
be  greatly  impeded  by  such  thickenings  upon  its  surface  and  along 
the  lines  of  the  trabeculae. 

Figs.  68  and  69  represent  a  species  of  pulmonary  fibrosis  which 
in  its  most  salient  features  is  different  from  the  forms  that  have 
been  considered.  The  lung  is  so  much  changed  as  to  be  almost  un- 


94  THE   ORIGIN   OF   DISEASE. 

recognizable.  It  has  lost  its  naturally  porous  and  open  appearance, 
and  is  nearly  solid.  The  vessels  are  thickened,  some  of  them  so 
much  that  the  calibres  are  almost  closed,  and  the  pleura  is  greatly 
thickened.  Such  tissue  is  not  like  that  which  grows  from  the  pleura 
and  fibrous  trabeculae  of  the  lung  in  pleurogenous  interstitial  pneu- 
monia, nor  has  it  any  resemblance  to  emphysema,  and  yet  there  is 
nothing  in  its  appearance  to  forbid  the  belief  that  the  region  had 
previously  been  emphysematous.  The  general  character  is  that  the 
lung  had  become  almost  evenly  solid.  There  are,  of  course,  remains 
of  the  natural  open  structure,  but  such  a  degree  of  solidity  could 
have  been  attained  only  by  a  universal  growth  of  the  fibrous  tissue 
which  composes  the  alveolar  walls,  thickening  them  and  in  most 
places  encroaching  upon  the  air-spaces  to  their  obliteration.  The 
thought  that  emphysema  might  have  been  the  forerunner  of  such 
generally  diffused  solid  fibrosis  is  interesting,  and  it  would  be  hard  to 
prove  that  such  was  not  the  case.  When  it  is  recollected  how  greatly 
morbid  fibrous  tissue  (cicatrix)  contracts  and  how  irresistible  this  ten- 
dency is,  it  seems  very  probable  that  portions  of  lung  which  had  been 
made  porous  but  fibrous  by  emphysema  might  sometimes  become 
more  fibrous  and  shrink  to  solidity,  if  other  disease  did  not  step  in 
to  kill  before  this  result  was  reached.  The  form  of  pulmonary  fibrosis 
illustrated  is  very  common  in  cases  of  Bright's  disease  of  long  stand- 
ing and  in  other  chronic  diseases  characterized  by  the  growth  of 
fibrous  tissue,  and  it  is  much  more  frequently  found  in  the  old  than 
in  young  persons.  Fig.  68  is  a  section  of  the  lung  of  a  woman 
sixty  years  old  who  died  of  Bright's  disease.  The  pleura  is  much 
thickened,  and  part  of  this  thickening  consists  of  material  like  that 
of  ordinary  fibromas,  such  as  are  common  upon  the  capsules  of 
organs,  while  at  other  areas  the  thickening  was  at  the  expense  of  the 
lung,  the  fibrous  growth  having  been  from  the  surface  downward 
into  the  lung.  The  pleura  is  bent  so  as  to  form  a  deep  sulcus  upon 
the  surface.  Fibrous  tissue  as  it  grows  is  apt  to  produce  such 
irregularities.  The  vessels  are  exceedingly  thick-walled,  and,  as  has 
already  been  said,  the  general  appearance  of  the  tissue  is  of  such 
solidity  that  it  no  longer  looks  like  lung.  Fig.  69  is  a  section  of 
the  lung  of  a  negro  woman  about  seventy  years  old  who  died  of 
fibrosis  of  the  heart,  lungs,  liver,  spleen,  and  kidneys  after  several 
years  of  feebleness  and  illness.  The  same  general  characteristics  are 
presented, — diseased  vessels,  thickened  pleura,  and  general  evenly  dif- 
fused fibrosis ;  but  besides  these  the  lung  is  pigmented,  and  there  is  a 


FIG.  68. — FIBROID  LUNG,     (x  16.) 

From  a  woman  of  sixty  years  who  died  of  Bright's  disease,  a  and  b  are  the  pleura, 
which  is  greatly  thickened,  and  there  is  a  deep  sulcus,  the  result  of  shrinking  and  twist- 
ing. At  a  the  thickening  is  of  the  pleura  itself,  while  at  b  the  growth  is  almost  entirely 
subpleural  and  has  taken  place  at  the  expense  of  the  lung.  The  blood-vessels  throughout 
the  lung  are  thick  and  partially  closed  by  endarterial  growth.  Most  of  the  tissue  is  a  dense 
fibrous  material  without  resemblance  to  the  open  loose-meshed  appearance  of  healthy  lung. 
Air-spaces  capable  of  having  performed  their  function  do  not  seem  to  be  present. 

FIG.  69.— FIBROID  LUNG.     (X  16.) 

From  a  negro  woman  of  about  seventy  years  who  died  having  fibrosis  of  the  heart,  lungs, 
liver,  spleen,  and  kidneys.  All  of  the  lung  included  is  very  fibroid,  there  being  no  natural 
alveoli,  z/,  a  vessel  with  thickened  walls.  Other  thick  vessels  are  included,  but,  as  they 
are  of  smaller  size,  they  are  not  easy  to  distinguish  without  greater  amplification.  py  the 
pleura,  which  is  greatly  thickened.  Below  g  there  is  a  mass  of  fibrous  tissue  in  the  lung 
which  is  continuous  with  the  pleura,  from  which  it  appears  to  extend  inward. 


THE   LUNGS.  95 

growth  of  fibrous  tissue  which  is  continuous  with  the  pleura  and  ex- 
tends from  it  deeply  into  the  lung.  A  fibrous  growth  extending  from 
the  pleura  into  the  lung  such  as  that  depicted  is  evidently  not  a  thick- 
ening of  one  of  the  pulmonary  trabeculae,  but  is  a  fibroid  invasion  of 
the  lung  tissue  itself,  which  is  liable  to  occur  at  any  part.  The  growth 
of  fibromas  upon  the  surfaces  of  organs,  the  ordinary  thickenings  of 
the  capsules,  and  the  extension  of  fibrous  growths  from  the  capsules 
into  the  organs  are  very  interesting  phenomena.  Whether  disease 
has  its  starting-point  in  such  growths,  or  whether  these  growths  are 
only  secondary  effects,  is  a  question  impossible  to  answer,  but  the 
answer  might  point  out  the  road  to  valuable  knowledge.  Fig.  70 
represents  a  phase  of  disease  entirely  different  from  any  heretofore 
shown.  It  is  from  the  wall  of  a  cavity  in  the  lung  of  a  man  twenty- 
six  years  old  who  had  pulmonary  phthisis  and  died  of  meningitis. 
Ordinarily,  tubercular  lung  tissue  is  fibro-cellular  and  is  more  or  less 
rich  in  cells  according  to  the  manner  of  its  growth.  In  the  portion 
of  lung  represented  the  pleura  is  thickened  and  somewhat  cellular, 
there  is  pigmentation,  and  the  cells  generally  are  large,  very  numerous, 
and  of  unusual  appearance,  many  of  them  having  the  protoplasm 
unstained,  and  in  some  there  is  no  nucleus.  They  are  of  the  same 
character  as  those  forming  the  new  growth  within  a  lung  arteriole 
already  described  (page  53).  Such  cells  are  peculiar  to  tissue  which 
was  of  very  rapid  growth.  The  amount  of  fibrous  material  is  less 
than  is  usual  in  tubercular  tissue,  and  there  are  two  peculiar  nests  of 
cells,  each  surrounded  by  a  fibrous  envelope.  The  cells  are  arranged 
in  a  somewhat  circular  manner,  or,  to  use  a  botanical  term,  whorled 
(the  drawing  does  not  make  this  very  clear).  The  appearance  is  very 
like  that  of  the  pearly  bodies  of  skin  cancer.  Circular  masses  of  cells 
of  this  character  are  common  in  the  healthy  skin  of  young  infants.  A 
similar  growth  of  cells  has  already  been  described  (Fig.  38)  which 
was  found  in  the  wall  of  a  minute  vein.  There  is  a  tendency  for  cells 
to  assume  this  circular  arrangement  when  there  has  been  rapid  growth. 
The  lesson  taught  is  that  these  circular  cell-nests  are  found  as  a 
result  of  diseased  growth  in  the  walls  of  veins,  in  skin  cancer,  in  the 
walls  of  tubercular  lung  cavities,  and  in  the  healthy  skin  of  young 
infants.  We  should,  therefore,  be  careful  how  we  ascribe  a  specific 
character  to  them. 

The  arteries  and  veins  of  the  lungs  are  naturally  much  thinner- 
walled  than  those  of  other  parts,  and  this  is  especially  true  of  the 
nutrient  vessels,  which  are  derived  principally  from  the  bronchial 


96  THE   ORIGIN   OF   DISEASE. 

arteries,  and  belong,  therefore,  to  the  systemic  circuit,  as  well  as  of 
the  pulmonary  arteries  and  veins.  The  thinness  of  the  walls  is  more 
noticeable  in  the  pulmonary  vessels  than  in  the  nutrient  branches 
because  of  their  larger  size. 

It  must  have  struck  every  one  who  has  been  present  at  many  post- 
mortem examinations  that  in  the  great  majority  of  instances  the  lungs 
contain  much  blood.  If  the  aid  of  the  microscope  is  invoked  and 
sections  are  examined,  it  is  the  exception  to  find  the  lung  of  any  one 
who  has  died  a  natural  death  without  a  greater  or  less  amount  of  blood 
lying  in  the  air-sacs.  Such  a  condition  is  always  the  result  of  disease, 
for  naturally  the  blood  should  be  inside  the  vessels  alone.  The 
amount  of  blood  in  the  pulmonary  alveoli  after  death  varies  infinitely. 
There  may  be  a  few  scattered  red  corpuscles,  or  the  spaces  may  be 
distended  with  them  so  as  to  be  impermeable  to  air.  Occasionally 
lungs  are  found  with  alveoli  entirely  filled  with  solid  masses  of  blood- 
corpuscles  except  the  most  central  portions,  which  remain  empty. 
The  appearance  of  such  specimens  is  peculiar.  In  tissue  stained 
with  carmine  the  blood  retains  the  yellowish-brown  color  which  it 
ordinarily  has  in  dead  tissues,  and  presents  the  appearance  of  many 
closely  appressed  circles  resembling  a  mass  of  frog's  eggs.  Such 
effusions  must  have  occurred  rapidly  during  the  last  few  hours  of  life, 
for  otherwise  there  would  be  some  evidence  of  separation  of  the  cor- 
puscles so  that  they  might  have  been  reabsorbed  or  have  been  dis- 
charged as  expectoration.  The  direct  cause  of  death  in  the  great 
majority  of  instances  is  effusion  into  the  lungs.  By  this  is  meant  that 
the  final  and  immediate  cause  of  death  is  the  escape  of  blood  and 
serum  into  the  lungs  to  such  an  extent  that  sufficient  air  to  maintain 
life  can  no  longer  be  obtained,  and  death  results  from  want  of  air  as 
much  as  it  does  in  a  man  who  is  seized  by  the  throat  and  his  windpipe 
closed  until  he  is  dead.  It  is  only  in  the  case  of  sudden  death  which 
results  from  the  cessation  of  action  of  the  brain  or  heart  that  the  lungs 
are  found  light  and  spongy  and  wholly  free  from  effusion.  Sudden 
death  may  result  from  the  destruction  of  the  brain  or  heart  by  injury, 
or  because  disease  causes  them  to  cease  suddenly  to  perform  their  func- 
tions. The  heart,  it  is  well  known,  may  instantly  cease  to  beat,  and 
death  result  in  a  few  moments,  and  the  brain,  as  a  result  of  a  tumor 
or  other  disease,  may  suddenly  cease  performing  its  function,  causing 
instant  death.  No  other  death  is  so  sudden  as  that  which  follows 
destruction  of  the  medulla  oblongata.  With  the  exception  of  those 
due  to  the  brain  or  the  heart,  it  may  be  said  that  all  other  deaths 


FIG.  70.— GROWTHS  IN  THE  WALL  OF  A  LUNG-CAVITY,  (x  250.) 
From  a  man  of  twenty-six  years  who  had  phthisis  and  died  of  meningitis,  o  are  the 
growths,  which  consist  of  nests  of  cells  not  unlike  those  of  the  growths  in  the  wall  of  a 
vein  depicted  in  Fig.  38.  d,  </is  the  lower  boundary  of  the  pleura,  which  is  much  thickened 
and  more  cellular  than  natural,  j  is  a  vessel  containing  blood-corpuscles,  t  indicates 
masses  of  pigment.  The  cells  of  which  the  tissue  is  composed  are  large,  and  many  of  them 
consist  ot  a  nucleus  surrounded  by  a  space  which  appears  to  be  empty,  and  outside  of  this 
is  the  cell-envelope.  The  appearance  of  other  cells  is  that  of  an  envelope  with  nothing 
inside  it. 


Fir;.  70. 


THE   LUNGS.  97 

result  from  the  lungs.  This  statement  for  all  practical  purposes  and 
from  the  stand-point  of  the  clinician  is  true,  although  physiologists 
will  describe  death  as  a  much  more  complicated  process. 

In  the  ordinary  acute  and  chronic  diseases  it  is  wonderful  how 
much  the  organs  can  bear.  Various  inflammations  may  exist,  the 
abdominal  cavity  may  be  filled  to  distention  with  liquid,  the  pericar- 
dium may  contain  serum,  the  heart  may  beat  with  extraordinary 
rapidity  or  the  greatest  irregularity,  the  lungs  themselves  may  be 
surrounded  by  liquid  in  the  pleura,  and  life  still  be  preserved,  but 
if  the  pulmonary  vessels  cease  to  perform  their  functions  and  allow 
the  transudation  of  much  blood  the  result  is  speedy  death. 

It  has  sometimes  been  thought  that  the  blood  found  in  the  air-cells 
resulted  from  post-mortem  transudation,  but  for  one  who  has  often 
watched  death  and  seen  that  the  only  sure  sign  of  its  near  approach 
is  the  filling  of  the  lungs,  and  that  this  always  occurs  unless  the  death 
is  sudden  from  the  heart  or  the  brain,  such  a  belief  is  unreasonable. 
The  condition  which  is  described  as  being  in  articulo  mortis  in  the 
vast  majority  of  instances  comes  on  only  when  the  contents  of  the 
pulmonary  vessels  begin  to  escape  into  the  lungs. 

The  observation  is  a  curious  one,  and  worthy  of  being  recorded, 
that  in  the  lung  effusion  of  blood  is  especially  liable  to  occur  directly 
beneath  the  pleura,  just  as  it  is  apt  to  occur  under  the  capsules  of 
other  organs,  as,  for  instance,  the  heart,  liver,  spleen,  and  kidneys. 
This  is  adverted  to  in  the  description  of  other  organs,  but  no  explana- 
tion of  it  can  be  found.  In  a  case  in  which  death  resulted  from  acute 
cholera  morbus  I  found  extensive  ecchymoses  beneath  the  capsules 
of  the  heart,  lungs,  liver,  and  kidneys.  Microscopical  examination 
showed  that  these  ecchymoses  had  no  depth,  that  they  did  not  pene- 
trate into  the  substance  of  the  various  organs,  but  lay  almost  entirely 
between  the  capsules  and  the  subjacent  tissues.  In  many  acute  and 
chronic  diseases  hemorrhage  beneath  the  capsules  of  the  organs  is 
frequently  found.  Associated  with  hemorrhages  beneath  capsules, 
and  evidently  a  part  of  the  same  process,  it  is  common  to  find  areas 
of  inflammation  or  of  pigmentation  and  thickening  of  the  capsules. 
Capsular  thickenings  are  frequently  the  seats  of  origin  of  disease,  as 
has  already  been  said,  inflammation  or  fibrosis  beginning  upon  the 
surface  and  extending  deeply  into  the  substance  of  the  lung.  The 
question  of  the  relation  of  pulmonary  fibrosis  to  consumption  of  the 
lungs  is  one  of  the  highest  importance;  it  is  discussed  elsewhere 
(page  89).  Lung  fibrosis  sometimes  coexists  with  amyloid  degenera- 

7 


98  THE   ORIGIN   OF   DISEASE. 

tion  of  the  other  organs,  and  it  is  hard  to  escape  from  the  belief  that 
they  are  allied  diseases  or  proceed  from  a  common  cause. 

The  lung,  like  all  the  other  organs,  is  liable  to  attacks  of  inflamma- 
tion, and,  as  has  already  been  pointed  out,  it  is  even  more  vulnerable 
than  any  of  the  other  organs,  for  the  reason  that  it  is  exposed  to  the 
direct  influence  of  the  atmosphere  with  which  it  is  constantly  filled. 
The  fact  has  also  been  mentioned  that  inflammatory  attacks  of  the 
lung  even  when  very  slight  in  character  may  pave  the  way  for  more 
severe  ones  subsequently,  though,  on  the  other  hand,  they  may  heal  so 
completely  as  to  leave  the  lung  for  all  practical  purposes  uninjured. 
From  what  is  known  of  the  general  behavior  of  the  process  of  in- 
flammation it  is  certain  that  the  exudative  material  deposited  in  the 
air-spaces  of  the  lungs  as  a  consequence  of  inflammation  is  sometimes 
imperfectly  removed  in  the  process  of  healing,  and  is  an  element  tend- 
ing to  produce  recurrent  inflammation  or  degeneration. 

Pneumonia  is  a  term  which  is  essential  to  describe  a  clinical  con- 
dition with  definite  pathological  changes  the  result  of  inflammation 
of  the  lungs,  and  which  in  its  typical  form  of  development  is  as  well 
defined  as  any  disease.  The  difficulties,  however,  of  the  physician 
and  pathologist  begin  when  the  attempt  is  made  to  decide  to  what 
extent  the  greatly  varied  forms  of  inflammation  of  the  lung  are  to  be 
included  by  the  term  pneumonia.  It  is  not  usual  at  present  to  classify 
all  inflammations  of  the  lungs  as  pneumonia,  and  on  this  account, 
and  because  pneumonia,  bronchitis,  sometimes  phthisis,  and  many  of 
the  chronic  degenerations  of  the  lungs  are  commingled,  the  employ- 
ment of  the  terms  at  present  in  use  to  describe  diseases  of  the  lungs 
is  often  exceedingly  unsatisfactory.  A  full  discussion  of  this  subject 
belongs,  however,  more  properly  to  the  head  of  diagnosis. 

Emphysema  is  so  intimately  connected  with  fibrosis  that  the  two 
must  often  if  not  always  be  classified  together.  It  occurs  at  all  periods 
of  life,  even  in  early  infancy  and  in  childhood,  as,  for  instance,  at  twelve 
years,  when  the  alveoli  may  be  found  enlarged  and  the  remaining 
fibrous  material  thickened  and  there  may  be  subacute  inflammation  of 
the  degenerated  part,  as  shown  by  the  presence  of  blood  and  exudate 
cells.  A  most  important  part  of  emphysema  is  the  decreased  vascu- 
larity  of  the  dilated  air-sacs.  Emphysema  seems  in  some  instances 
to  serve  a  conservative  purpose  in  chronic  conditions  of  disease.  For 
instance,  in  an  old  case  of  gouty  Bright's  disease,  in  which  there  were 
obliteration  of  the  pleural  sacs  by  adhesion,  great  fibrosis,  and  emphy- 
sematous  enlargement  of  the  air-sacs,  life  was  unusually  prolonged, 


THE   LUNGS.  99 

and  it  seemed  as  though  this  was  due  to  the  fact  that  the  lungs  did 
not  fill  up  and  cause  death  in  the  usual  way.  The  lung  could  not 
collapse,  as  it  was  held  open  by  the  pleural  adhesions,  and  its  sub- 
stance was  spongy  and  leathery  and  avascular  to  such  an  extent  that 
it  seemed  not  to  have  had  sufficient  vitality  to  fill  up  and  cut  off  the 
supply  of  oxygen.  This  has  been  mentioned  also  in  connection  with 
Fig.  66,  which  shows  large  emphysematous  sacs  remaining  empty 
while  surrounded  by  tissue  partly  solidified  from  inflammation.  The 
blood-vessels  are  very  commonly  thickened.  By  practice  lesser  de- 
grees of  emphysema  and  fibrosis  may  be  recognized  by  any  one  accus- 
tomed to  search  for  them,  both  with  the  unaided  eye  and  in  sections 
for  microscopical  examination. 

Pigmentation  of  the  lungs  exists  to  a  greater  or  less  extent  in  all 
persons  subjected  to  the  conditions  of  modern  civilization,  the  par- 
ticles suspended  in  the  atmosphere  being  inhaled  and  lodging  in 
the  lungs :  besides,  it  is  possible  that  pigment  is  carried  to  the  lungs 
and  deposited  in  them  by  the  circulation.  It  is  so  very  common  to 
find  a  mass  of  pigment  lying  in  and  appearing  to  be  the  centre  of  irri- 
tation in  a  tubercular  area  or  in  a  spot  of  subpleural  inflammation,  that 
it  seems  to  me  that  pigment  in  the  lungs  is  by  no  means  so  harmless 
as  it  is  commonly  thought  to  be.  Like  any  other  foreign  body  in  the 
tissues,  pigment  must  either  become  encapsulated  and  lie  quiescent 
or  must  form  the  centre  of  an  inflammation.  It  is  highly  probable, 
therefore,  that  a  deposit  of  pigment  is  much  more  frequently  the 
source  of  disease  than  is  generally  supposed. 

A  common  post-mortem  condition  is  the  presence  of  calcareous 
deposits  in  the  lung ;  these  may  be  either  near  the  surface  or  deeply 
seated  in  the  organ,  and  generally  the  tissue  is  somewhat  puckered 
and  contracted  around  the  chalky  material.  Such  deposits  are  more 
frequently  found  in  elderly  persons  and  in  those  who  have  been  long 
the  subjects  of  chronic  disease.  It  has  been  commonly  taught  that 
the  deposit  of  chalk  in  the  lung  and  the  surrounding  puckering  of 
tissue  are  to  be  looked  upon  as  signs  that  the  person  had  previously 
suffered  with  phthisis,  and  that  there  had  been  a  cavity  in  the  lung 
which  in  healing  had  puckered  the  tissue  and  caused  the  deposit  of 
the  chalk.  Such  a  conclusion  has  seemed  to  me  not  to  be  warranted 
by  the  facts.  Although  the  deposit  of  chalk  in  tubercular  portions 
of  lung  is  common  enough,  on  the  other  hand,  calcareous  material 
is  so  very  frequently  found  in  other  organs  and  tissues  of  the  body 
in  places  and  under  circumstances  that  make  it  certain  that  it  had 


ioo  THE   ORIGIN   OF   DISEASE. 

nothing  to  do  with  tubercular  disease,  and  the  appearance  of  the 
chalky  deposits  in  the  lungs  is  so  little  suggestive  of  tuberculosis, 
either  present  or  past,  as  to  make  it  seem  more  likely  that  chalk  in 
the  lungs  is  only  the  result  of  disordered  action  of  the  organism 
which  allowed  the  blood  to  cause  it,  just  as  such  disordered  action 
may  cause  the  deposits  in  other  places,  and  that  generally  it  is  in  no 
wise  related  to  tuberculosis. 

It  seems  almost  superfluous  to  say  that  of  all  the  pathological 
changes  that  the  lungs  undergo  those  produced  by  consumption  are 
the  most  important.  It  is,  in  temperate  climates,  the  cause  of  the 
death  of  a  greater  number  of  people  than  any  other  disease.  This  is 
not  the  place  to  discuss  in  full  the  questions  of  consumption  of  the 
lungs,  pulmonary  phthisis,  and  tuberculosis.  Here  all  that  is  neces- 
sary is  to  state  briefly  something  of  the  character  of  the  lesions. 
The  appearances  of  the  grosser  lesions  of  destruction  and  of  the 
smaller  tubercles  or  of  miliary  tubercles  are  unmistakable,  and  so 
are  those  of  sections  of  tissue  from  typically  consumptive  lungs  when 
examined  with  the  microscope.  On  the  other  hand,  if  the  question 
is  looked  at  from  a  different  stand-point,  there  is  nothing  whatever  in 
such  tissue  which  is  peculiar  to  it,  unless  it  be  the  presence  of  giant 
cells  or  tubercle  bacilli.  The  point  it  is  desired  to  emphasize  is  that 
tubercular  tissue  is  nothing  but  a  growth  of  fibrous  and  cellular  mate- 
rial in  which  one  or  other  of  the  two  constituent  parts  preponderates 
according  as  the  growth  has  been  rapid  or  slow.  Much  fibrous  tissue 
and  few  cells  are  found  if  the  growth  has  been  slow,  and,  on  the  other 
hand,  there  are  many  cells  and  little  fibrous  tissue  if  the  growth  has 
been  rapid,  exactly  as  is  the  case  in  cancers,  in  which  the  scirrhous 
and  encephaloid  forms  constitute  the  two  extremes.  Giant  cells  and 
tubercle  bacilli  are  the  only  specific  things  which  are  peculiar  to  tuber- 
cular tissue.  So  far  as  concerns  bacilli,  they  often  cannot  be  found  in 
a  given  piece  of  tissue  which  is  known  to  be  tubercular.  Giant  cells 
are  not  understood.  Even  now  no  one  knows  what  they  are,  although 
there  is  every  reason  to  suppose  from  their  appearances  and  behavior 
that  they  are  a  result  of  distorted  tissue-growth  and  are  not  of  extra- 
neous origin.  It  is  certain  that  practically  it  often  happens  that  in 
tissue  undoubtedly  tubercular  neither  giant  cells  nor  bacilli  can  be 
found.  Sometimes  the  most  careful  examination  will  fail  to  show 
whether  a  particular  specimen  was  tubercular  or  not ;  but  the  point  of 
greatest  importance  is  that  structurally  tubercle  is  only  a  fibre-cellular 
growth,  and  that  it  is  not  subject  to  any  greater  variation  of  appearance 


THE   LUNGS.  101 

than  other  diseased  tissues.  Young  tubercle  is  different  from  old,  and 
that  of  rapid  growth  is  unlike  that  which  was  slow  in  growing.  The 
greatest  difference  perhaps  is  between  that  which  has  begun  to  disin- 
tegrate and  that  which  is  still  active,  but  in  saying  this  all  has  been 
said,  and  the  fact  remains  that  consumption  of  the  lungs  and  all  forms 
of  tuberculosis  are  morphologically  only  the  growth  of  fibro-cellular 
tissue  and  its  destruction. 


CHAPTER    VII. 

THE    LIVER. 

As  the  liver  is  the  largest  secreting  organ  of  the  body,  there  is 
every  reason  to  suppose  its  function  is  of  the  highest  importance ;  the 
consequences,  therefore,  of  any  derangement  of  it  are  likely  to  be 
serious.  At  the  same  time  it  stands  to  reason  that  an  organ  which  is 
so  large  and  so  vascular  must  be  exceedingly  liable  to  disease.  The 
condition  of  the  liver  in  early  infancy  is  quite  different  from  its  con- 
dition in  later  life.  During  infancy  it  is  softer  and  of  a  different 
color.  When  examined  with  the  microscope  it  appears  to  be  com- 
posed of  an  even  mass  of  cells,  rich  in  nuclei  and  giving  the  impres- 
sion of  an  activity  of  growth  which  does  not  exist  in  older  tissue, 
and  there  is  but  little  fibrous  tissue.  Notwithstanding  the  great 
difference  between  the  young  and  the  old  organ,  hepatic  disease  of 
chronic  form,  such  as  is  most  common  in  middle  life  or  in  old  age, 
may  occur  in  the  young.  Disease  of  this  character  I  have  found  as 
early  as  the  fifth  month  of  life,  and  at  nine,  ten,  twelve,  and  fourteen 
years.  Chronic  inflammation  and  cirrhosis  or  fibrosis  are  types  of 
the  class,  being  common  in  middle  life  and  in  old  age.  When  they 
occur  in  children  or  infants  they  are  generally  accompanied  by  an 
appearance  of  premature  age. 

The  commonest  morbid  change  of  the  liver  found  after  death  is 
that  named  nutmeg  liver.  This  condition  is  very  frequent  in  cases  of 
long-standing  heart  disease;  it  is  generally  attributed  to  obstruction 
of  the  circulation,  and  is  called  mechanical  hyperaemia  of  the  liver. 
Rindfleisch  mentions  with  approval  and  makes  use  of  the  name  given 
it  by  Virchow,  of  red  atrophy.  Although  it  is  true  that  the  disease 
is  exceedingly  common  in  cases  of  heart  disease  in  which  there  has 
long  been  obstruction  of  the  circulation,  it  seems  to  be  going  further 
than  is  warranted  by  the  facts  to  assume  that  it  never  exists  under  any 
other  circumstances  and  that  it  is  always  due  to  passive  congestion. 
The  disease  is  represented  in  typical  form  by  Figs.  71,  72,  and  73. 
The  first  includes  part  of  a  portal  vein  with  a  small  branch  of  the 
hepatic  artery  and  a  minute  bile-duct.  Around  these  are  grouped 
several  acini,  which  show  different  conditions  of  degeneration  charac- 

102 


FIG.  71. — DEGENERATION  OF  THE  LIVER  COMMONLY  CALLED  NUTMEG  LIVER,     (x  50.) 

From  a  negro  man  of  thirty  years  who  died  of  organic  heart  disease.  The  large  space 
in  the  centre  of  the  picture  is  the  opening  of  a  portal  vein.  The  acinus  r  at  its  centre 
has  no  secreting  cells  left.  TV  indicates  the  area  depicted  more  highly  magnified  by  Fig. 
73.  s  is  an  acinus  like  r,  but  that  the  liver  framework,  from  which  the  secreting  cells  have 
disappeared  at  the  central  portion,  is  filled  with  blood-corpuscles.  A  condition  parallel  to 
this,  but  from  another  section,  is  shown  by  Fig.  72.  q  is  an  acinus  in  which  the  tissue  is 
much  broken  and  full  of  holes  ;  these  are  cysts,  for  they  are  larger  than  fat-cells  and  are 
unlike  them. 


FIG.  71. 


w 


FIG.  72. — NUTMEG  LIVER,     (x  280.) 

From  a  negro  man  of  thirty  years  who  died  of  organic  disease  of  the  heart,  a  is  a  por- 
tion of  tissue  from  near  the  centre  of  an  acinus.  Everything  is  overwhelmed  with  blood,  the 
trabeculae  which  formerly  contained  liver  cells  as  well  as  the  natural  blood-channels  being 
filled  to  their  utmost  capacity  with  corpuscles.  Nothing  remains  of  the  liver  tissue  but 
the  few  scattered  cells,  which  are  in  appearance  precisely  similar  to  those  commonly  seen 
in  urine  and  occasionally  in  cysts.  A  striking  feature  is  that  the  portion  of  the  liver  which 
is  the  most  indestructible  and  the  only  portion  which  has  persisted  is  what  may  fittingly 
be  called  the  skeleton, — namely,  the  fibrous  material  forming  the  walls  of  the  trabeculae. 
This  is  composed  of  tubes  into  which  were  packed  the  secreting  cells.  It  appears  in  the 
picture  as  strong  fibrous  lines,  of  which  two  run  parallel  to  each  other,  forming  the  two 
sides  of  the  trabecula.  b  is  a  region  in  which  the  liver  substance  is  disintegrating  ;  it  con- 
sists of  granular  matter  and  secreting  cells  in  various  stages  of  destruction.  Perpendicu- 
larly from  top  to  bottom  the  picture  is  divided  ;  to  the  left  is  the  region  overwhelmed  by 
blood,  the  central  portion  of  the  acinus,  while  to  the  right  the  liver  tissue  persists,  the 
peripheral  portion  of  the  acinus,  c  is  a  trabecula  in  which  the  process  of  destruction  and 
atrophy  of  the  liver  cells  can  be  seen.  The  fibrous  walls  of  the  trabecula  are  distinct ;  in 
the  centre  is  the  cord  of  liver  cells,  only  a  single  row  remaining,  and  these  are  so  small 
and  so  much  rounded  by  pressure  that  if  they  were  isolated  they  would  not  be  recog- 
nizable as  liver  cells.  Between  the  fibrous  walls  and  the  secreting  cells  there  is  a  space 
which  contains  debris  and  blood-corpuscles,  the  blood  having  escaped  from  its  natural 
channels  and  forced  its  way  into  the  trabecula  to  destroy  the  secreting  cells. 

FIG.  73. — NUTMEG  LIVER.     (X  280.) 

The  region  w  from  Fig.  71,  more  highly  magnified.  A  beautiful  demonstration  of 
the  common  appearances  of  nutmeg  liver  when  the  process  has  reached  a  more  advanced 
stage  than  that  represented  by  Fig.  72.  Blood-corpuscles  are  no  longer  to  be  seen  in  the 
diseased  portion,  where  only  the  skeleton  of  liver  remains.  Were  a  line  drawn  from  a  to 
b,  it  would  divide  the  picture  so  that  the  tissue  from  the  periphery  of  the  acinus  would  lie 
below  and  that  from  the  centre  above  the  line.  The  latter  consists  of  the  liver  framework 
containing  still  some  partially  destroyed  cells.  Close  examination  enables  one  to  follow 
the  remains  of  trabeculae  upward  from  the  sound  into  the  diseased  portions. 


Fig. 7 2 


THE  LIVER.  103 

teristic  of  the  disease.  The  tissue  is  unlike  healthy  liver  in  one  re- 
spect :  instead  of  being  well  knit,  there  are  numerous  holes,  which 
produce  an  open  appearance.  In  one  of  the  acini  (see  description  of 
Fig.  71)  the  holes  are  so  large  and  the  mesh-work  so  open  that  cystic 
degeneration  is  strongly  suggested.  Such  appearances  could  not  be 
due  to  fatty  degeneration.  The  existence  of  these  holes  is  not  usually 
mentioned  in  the  descriptions  of  nutmeg  liver,  and  yet  they  are  in- 
variably present  and  its  most  characteristic  feature.  Before  it  is  reason- 
able to  accept  the  congestion  theory  as  a  complete  explanation  of 
nutmeg  liver  it  is  necessary  to  find  a  reason  for  the  existence  of  the 
holes,  and  such  a  reason  is  not  supplied  by  the  assertion  either  that 
they  are  dilated  blood-spaces  or  that  they  are  the  result  of  fatty  de- 
generation. This  matter  is  further  discussed  in  connection  with  the 
subject  of  cystic  disease  of  the  liver  (page  106).  Two  of  the  acini  in- 
cluded in  the  low-power  drawing  (Fig.  71)  demonstrate  the  ordinary 
microscopical  appearances  of  nutmeg  liver.  In  one  the  secreting  cells 
have  entirely  disappeared  from  the  centre  of  the  acinus,  leaving  only 
the  framework  of  the  hepatic  tissue  behind.  In  the  other  also  the 
liver  cells  have  disappeared  at  the  centre,  but  their  place  has  been 
taken  by  a  solid  mass  of  blood-corpuscles. 

The  two  drawings  made  with  greater  amplification  (Figs.  72  and  73) 
show  the  character  and  details  of  such  degeneration  better  than  the 
low-power  drawing,  in  which  the  enlargement  was  not  sufficient  to 
show  individual  blood-corpuscles.  The  upper  picture  represents  liver 
which  appears  as  if  overwhelmed  by  blood.  To  the  left  there  are  to 
be  seen  only  the  framework  of  the  liver  and  a  mass  of  blood-corpus- 
cles containing  a  few  scattered  cells.  To  the  right  the  liver  cells  still 
remain.  In  the  midst  of  these  cells  is  a  column  or  trabecula  of  the 
secreting  cells  (see  description  of  Fig.  72,  c\  which  demonstrates  the 
process  by  which  they  become  extinguished.  Blood-corpuscles  have 
insinuated  themselves  between  the  liver  cells  and  the  fibrous  frame- 
work, which  in  healthy  liver  is  entirely  filled  by  the  cells.  The  tra- 
beculae  generally  consist  of  a  double  row  of  secreting  cells,  instead 
of  a  single  one  as  this  does.  The  ordinary  shape  of  liver  cells  is  well 
known,  and  most  of  those  in  the  picture  have  it,  but  those  of  the 
column  mentioned  are  rounded  and  so  distorted  that  they  could  not 
be  recognized  as  liver  cells  were  they  isolated.  The  process  appears 
to  be  one  in  which  the  blood-corpuscles  escape  from  the  interior  of 
the  vessels  and  are  forced  into  the  tissue.  They  must  crush  the  deli- 
cate secreting  cells,  causing  their  disappearance  and  leaving  the  fibrous 


104  THE   ORIGIN   OF   DISEASE. 

framework  or  skeleton  of  the  trabeculae  filled  with  blood.  There  are 
also  included  in  the  picture  a  few  of  the  holes  in  the  tissue  which 
have  already  been  mentioned  as  constituting  one  of  the  most  striking 
features  in  the  low-power  drawing  of  nutmeg  liver.  The  lower 
picture  (Fig.  73)  is  an  enlarged  view  of  a  portion  of  one  of  the  acini 
included  in  the  low-power  drawing  (Fig.  71).  Half  of  it  represents 
liver  tissue  which  is  normal,  except  that  there  are  more  large  open 
spaces  than  is  natural,  while  the  other  half  is  made  of  liver  frame- 
work from  which  almost  all  the  secreting  cells  have  disappeared. 
The  persistence  of  the  framework  or  skeleton  of  the  liver  after  the 
secreting  cells  have  disappeared  is  remarkable,  but  perhaps  it  is  only 
what  should  be  expected,  considering  that  it  is  composed  of  a  hard 
fibrous  material  less  easily  destroyed  than  the  softer  secreting  cells. 
The  assumption  that  all  this  destruction  is  the  result  of  congestion 
and  is  caused  by  an  overflowing  of  the  tissue  by  the  blood  seems  un- 
tenable. The  extent  to  which  such  liver  tissue  can  be  regenerated  is 
an  important  question,  which  cannot  be  satisfactorily  answered  at  pres- 
ent. The  appearances  which  have  been  described  are  the  well-known 
ones  of  nutmeg  liver,  or,  if  the  name  be  preferred,  of  red  atrophy, 
and  the  open  spaces  or  holes  which  have  been  mentioned  are  always 
to  a  greater  or  less  extent  found  as  an  accompaniment  of  the  disease. 
Figs.  74  and  75  show  the  same  holes,  but  under  conditions  and  of 
an  appearance  different  from  those  already  described.  The  two  por- 
tions of  liver  depicted  lay  close  together,  and  both  contain  many  of 
the  open  spaces.  In  one  the  tissue  is  filled  with  blood-corpuscles, 
while  in  the  other  none  are  visible.  The  hemorrhage  was  very  great, 
and  this  is  well  shown  by  the  drawing.  The  blood-spaces  are  all  dis- 
tended, and  even  the  secreting  cells  were  invaded.  Blood-corpuscles 
seem  to  cover  everything,  and  it  looks  as  if  they  had  forced  themselves 
even  into  the  substance  of  the  secreting  cells.  There  is,  however,  one 
striking  exception  to  this :  most  of  the  holes  remain  empty,  the  blood 
having  been  unable  to  break  through  their  envelopes  to  fill  them. 
Many,  however,  are  visible  which  are  full  of  blood-corpuscles  like  the 
rest  of  the  tissue.  That  the  holes  here  shown  and  those  in  the  liver 
which  had  undergone  nutmeg  degeneration  are  of  the  same  nature 
does  not  admit  of  doubt,  and  yet  the  patients  and  their  diseases  and 
modes  of  death  could  hardly  have  been  more  different  than  they  were. 
The  patients  from  whom  Figs.  72  and  73  were  taken  were  both 
negro  men  thirty  years  of  age  who  died  of  heart  disease  with  typical 
nutmeg  livers,  while  Figs.  74  and  75  are  of  the  liver  of  a  prematurely 


FIG.  74. — CYSTIC  DISEASE  OF  THE  LIVER,     (x  280.) 

From  a  woman  of  sixty  years  who  died  of  Bright's  disease  and  had  cirrhosis  of  the  liver. 
Fig.  84  is  from  the  same  case.  The  large  spaces  are  the  cysts  ;  some  of  them  contain 
amorphous  material  and  an  ill-defined  nucleus,  but  these  are  the  smaller  ones,  those  of 
larger  size  generally  appearing  to  be  empty. 

FIG.  75. — CYSTIC  DISEASE  OF  THE  LIVER,     (x  280.) 

From  the  same  section  as  Fig.  74 ;  an  adjacent  region.  Blood  has  overwhelmed  the 
tissue ;  the  capillary  spaces  are  distended  with  red  blood-corpuscles ;  the  liver  cells  are 
filled  or  overlaid  or  underlaid  by  the  corpuscles ;  they  even  fill  most  of  the  cystic  spaces, 
only  a  few  remaining  empty. 

FIG.  76. — CYSTIC  DISEASE  OF  THE  LIVER,     (x  55-) 

A  collection  of  irregularly  divided  cysts  surrounded  by  liver  tissue  ;  from  a  man  fifty- 
one  years  of  age  who  died  of  perihepatic  abscess.  At  h  the  columns  of  secreting  cells 
have  been  compressed  by  the  growing  cysts  so  that  they  are  much  narrowed,  g,  a  region 
presenting  the  ordinary  appearances  of  fatty  degeneration,  the  oil-cells  being  of  large  size. 
a  corresponds  with  x,  b  with  y,  and  c  with  z,  in  Fig.  77,  which  is  a  representation  of  the 
same  region  more  highly  magnified. 

FIG.  77. — CYSTIC  DISEASE  OF  THE  LIVER,     (x  280.) 

A  more  highly  magnified  view  of  a  portion  of  Fig.  76 ;  a,  b,  and  c  in  the  latter  are 
indicated  by  x,  y,  and  z  respectively,  x  and  y  are  two  cysts  with  a  broken  wall  of  separa- 
tion. At  e  the  cyst-wall  is  composed  of  partly  degenerated  liver  cells,  and  much  of  the 
wall  is  of  this  nature,  although  at  places  there  is  some  fibrous  material,  z  is  the  central 
one  of  three  cavities  which  are  too  large  to  be  ordinary  fat-cells,  n,  a  nucleus  in  the  wall 
of  one  of  the  cavities  ;  the  appearance  is  that  generally  given  as  typical  of  fatty  degen- 
eration of  a  liver  secreting  cell,  y*  presents  the  appearances  typical  of  fatty  degeneration 
of  a  liver  cell,  and  surrounding  it  are  others  in  various  stages  of  the  same  process  of  de- 
struction. It  seems  as  if  _/",  z,  and  y  must  represent  progressively  increasing  stages  of  the 
same  process  of  cystic  destruction  of  liver. 


THE   LIVER.  105 

aged  woman  of  sixty  who  died  of  Bright's  disease  with  fibrosis  of  the 
heart,  lungs,  and  spleen,  and  whose  liver  was  typical  of  cirrhosis  of 
the  contracting  form.  It  might  be  thought  that  the  holes  in  both 
cases  resulted  from  fatty  degeneration,  which  is  well  known  to  be  a 
usual  accompaniment  of  both  forms  of  disease.  Their  appearance, 
however,  and  their  large  size  forbid  such  an  assumption. 

Existing  classifications  of  disease  are  inadequate  to  satisfy  a  mind 
that  seeks  precision.  Diseases  that  are  commonly  considered  to  be  as 
far  apart  as  nutmeg  liver,  fatty  changes,  cystic  disease,  hypertrophic 
cirrhosis,  and  cirrhosis  of  the  contracting  form  present  so  many 
common  features  that  it  is  impossible  not  to  believe  that  they  are 
all  related,  or  that  there  may  be  a  common  cause  or  causes  which 
produce  them  all.  This  relationship  can  be  best  explained  by  illus- 
trating the  anatomy  of  the  fatty,  cystic,  and  cirrhotic  changes  be- 
fore the  subject  of  the  general  connection  of  the  various  diseases  is 
discussed.  It  must  be  kept  in  mind  that  the  holes  in  the  liver  here- 
tofore demonstrated  cannot  be  satisfactorily  accounted  for  either  as 
being  blood-channels  or  as  due  to  fatty  degeneration,  nor  can  their 
presence  in  nutmeg  livers  be  explained  by  the  hypothesis  that  the 
disease  is  the  result  of  passive  congestion. 

Figs.  76  and  77  are  pictures  of  the  liver  of  a  man  of  fifty-one  years 
who  died  of  perihepatic  abscess.  The  first  is  a  low-power  view,  and 
the  second  represents  a  small  portion  of  the  same  field  more  highly 
magnified.  (See  description.)  The  low-power  drawing  shows  a  num- 
ber of  large  irregularly  divided  cavities  surrounded  by  liver  tissue  in 
which  the  columns  of  cells  have  been  flattened,  and  in  which  to  the 
right  and  left  of  the  large  cavities  there  are  areas  showing  typical  fatty 
degeneration  of  the  secreting  cells.  The  large  cavities  are  cysts.  Fig. 
77,  having  been  drawn  with  greater  amplification,  shows  more  of  the 
details  of  structure.  The  cysts,  two  of  which  are  included,  are  con- 
nected, as  the  separating  wall  is  broken.  Their  surrounding  walls  are 
composed  of  irregular  and  flattened  liver  cells  and  shreds  of  fibrous 
tissue.  Their  size  and  appearance  make  it  certain  that  they  were 
cysts  and  had  contained  a  watery  fluid,  not  oil.  There  are  also  in- 
cluded a  number  of  cells  showing  typical  fatty  degeneration.  Small 
oil-globules  having  developed  within  the  cell  envelope,  the  appearance 
presented  is  of  an  oil-globule  surrounded  by  a  ring  which  is  composed 
of  the  liver  cell,  and  in  this  the  nucleus  often  is  distinctly  visible. 
There  are  a  few  of  these  oil-globules  (see  description  of  plate)  which 
are  of  much  larger  size  than  the  ordinary  ones  of  fatty  degeneration, 


106  THE   ORIGIN   OF   DISEASE. 

and  yet  much  smaller  than  the  cysts  shown  in  the  drawing.  Careful 
consideration  of  the  appearances  of  the  pictures  and  of  the  tissue  from 
which  they  were  made  forces  upon  the  mind  the  question  whether 
all  these  cavities  may  not  be  only  different  gradations  of  the  same 
disease,  and  whether  from  the  smallest  globule  of  fat,  which  as  seen 
with  the  microscope  looks  like  an  empty  space,  to  the  largest  cavity 
in  the  tissue,  they  are  not  only  the  progressive  stages  of  one  process 
which  has  ended  in  cystic  degeneration. 

Cystic  degeneration  of  the  liver  is  generally  considered  rare  and 
something  of  a  pathological  curiosity.  Cysts  of  large  size  are  not  of 
frequent  occurrence  in  the  liver,  but  in  my  experience  small  ones  are 
not  unusual.  By  this  are  meant  cysts  of  such  size  as  those  which 
have  been  shown,  or  even  smaller,  being  so  small  that  they  might 
elude  detection  by  the  naked  eye,  although  if  by  accident  included  in 
a  section  they  would  be  very  striking  when  seen  with  the  microscope. 
The  theory  has  been  put  forward  and  very  generally  accepted  that 
cysts  in  the  liver  have  their  origin  in  obstruction  and  consequent  dila- 
tation of  the  bile-ducts.  It  is  not  possible  to  prove  this  theory  incor- 
rect, but  some  time  ago  I  published  an  account  of  a  case  *  of  cystic 
degeneration  of  the  heart,  spleen,  liver,  and  kidneys  in  which  it  was 
shown  that  there  is  ground  to  suppose  that  such  cysts  originate  in  the 
capillaries.  True  cysts,  according  to  the  classifications,  are  those  which 
had  their  origin  in  the  dilatation  of  a  previously  existing  duct  or 
cavity,  while  false  cysts  are  those  developed  directly  in  the  meshes  of 
a  tissue,  such  as  abscesses  or  blood-extravasations.  That  the  cysts 
in  four  different  organs  in  the  case  mentioned  were  true  and  not  false 
cysts  was  shown  by  their  appearances.  It  is  in  the  highest  degree 
probable  that  they  were  all  of  the  same  nature, — that  their  mode  of 
origin  in  one  organ  was  their  mode  of  origin  in  all.  In  the  heart  and 
spleen  there  exist  no  ducts  or  cavities  in  which  cysts  could  arise 
except  the  blood-vessels  or  lymphatics.  Cystic  enlargements  of  blood- 
vessels are  common  enough,  while  almost  nothing  is  known  of  the 
origin  of  such  disease  in  lymphatics.  The  probability,  therefore,  that 
the  cysts  in  the  heart  and  spleen  had  their  origin  in  the  blood-vessels 
is  very  great.  If  they  arose  in  the  blood-vessels  in  the  heart  and 
spleen,  it  is  most  likely  they  had  the  same  origin  in  the  liver  and 
kidneys.  This  train  of  reasoning,  though  it  proves  nothing,  leads  up 
to  the  assertion  that  in  the  case  of  cystic  disease  under  consideration 

*  Journal  of  Anatomy  and  Physiology,  vol.  xxvi.  p.  454. 


FIG.  78. — CYSTIC  LIVER.     (X  5-) 

From  a  man  of  seventy-seven  years  who  had  also  cystic  disease  of  the  heart,  spleen, 
and  kidneys.  The  cysts  are  of  various  sizes  and  generally  appear  empty,  but  some  contain 
amorphous  material  (c}.  Some  of  the  cysts  have  well-defined  fibrous  walls,  in  others  the 
boundaries  are  liver  cells.  This  is  better  shown  by  Fig.  79,  which  is  the  area  b  more  highly 
magnified.  » 

FIG.  79. — CYSTIC  LIVER,     (x  45-) 

The  area  b  in  Fig.  78,  more  highly  magnified.  <•/,  amorphous  cyst-contents  ;  <?,  fibrous 
cyst- walls ;  f,  liver  cells  separating  one  cyst  from  another.  There  is  great  increase  of 
fibrous  tissue  ;  g  is  an  island  of  liver  cells  surrounded  by  fibrous  tissue.  The  columns  of 
secreting  cells  have  been  flattened  and  narrowed  by  the  fibro-cystic  growth. 


FIG.  78. 


THE   LIVER.  107 

it  is  more  reasonable  to  believe  that  the  cysts  in  the  liver  and  kidneys 
had  their  origin  in  the  blood-vessels  than  in  the  hepatic  and  renal 
ducts,  as  is  commonly  assumed  to  be  the  case. 

Figs.  78  and  79  represent  a  portion  of  the  liver  from  the  case  of 
cystic  disease  under  discussion.  The  patient  was  a  man  seventy-seven 
years  old  who  had  lived  an  irregular  life  and  was  a  hard  drinker.  The 
low-power  drawing  shows  the  size  of  the  cysts  and  that  they  were 
very  numerous.  The  details  of  structure  are  better  seen  in  the  picture 
drawn  with  greater  amplification.  This  shows  the  amorphous  and 
shreddy  nature  of  the  material  which  was  contained  by  some  of  the 
cysts,  and  that  their  walls  were  made  up  partly  of  fibrous  tissue, 
sometimes  mere  fibrous  threads  separating  one  cavity  from  another, 
and  again  that  the  liver  cells  themselves  constituted  the  cyst-walls. 
The  columns  of  liver  cells  are  seen  in  places  to  have  been  flattened 
by  the  pressure  of  the  growth  of  the  cysts  or  of  the  fibrous  tissue, 
or  of  both.  An  important  point  to  be  noticed  is  that  there  has  been 
an  extensive  growth  of  morbid  fibrous  tissue,  and  it  should  be  re- 
membered that  fibrosis  seems  to  be  an  invariable  accompaniment  of 
cystic  disease  of  the  liver.  In  hepatic  fibrosis  it  is  common  for  the 
fibrous  tissue  to  form  in  such  a  way  as  to  surround  a  group  of  the 
secreting  cells,  so  that  the  appearance  is  of  an  island  of  liver  cells 
surrounded  by  the  sweeping  lines  of  morbid  fibrous  tissue.  This 
appearance  is  never  seen  in  natural  liver.  Such  an  island  is  included 
in  the  drawing  (Fig.  79). 

Figs.  80,  8 1,  82,  and  83  are  from  the  liver  of  a  man  forty-seven 
years  old  who  died  of  the  disease  which  has  been  named  Charcot's 
hypertrophic  cirrhosis  of  the  liver.  The  peculiarities  of  this  disease 
are  the  growth  of  fibrous  tissue,  the  enlargement  of  the  liver,  which 
is  sometimes  very  great,  and  the  formation  of  new  bile-ducts.  In  the 
case  under  discussion  the  liver  was  fibroid  and  enormously  enlarged, 
and  it  presented  the  appearances  which  are  commonly  considered  to 
denote  the  formation  of  new  bile-ducts.  The  pictures  upon  the  plate 
show  these  well-known  lesions,  but  they  also  demonstrate  the  exist- 
ence of  other  pathological  lesions  which  are  usually  supposed  not  to 
have  any  relation  to  the  disease.  Their  study  is  both  interesting  and 
highly  instructive. 

Fig,  80  is  a  cyst  surrounded  by  fibrous  tissue.  At  one  side  in  its 
wall  there  was  a  deposit  of  calcareous  material, — very  well  shown  by 
the  drawing.  The  cyst  was  sufficiently  large  to  be  easily  seen  with 
the  naked  eye,  and  was  surrounded  with  yellowish,  degenerated  mate- 


io8  THE   ORIGIN   OF   DISEASE. 

rial.  It  lay  quite  close  to  the  capsule  of  the  liver,  and  in  fibrous  tissue 
which  had  grown  directly  under  and  was  continuous  with  the  capsule. 
This  morbid  fibrous  material  presents  an  open-meshed  appearance,  the 
holes  being  so  large  as  to  suggest  that  the  tissue  was  all  in  such  a 
condition  that  there  was  a  tendency  to  the  development  of  numerous 
cysts.  Another  cyst  is  included  which  is  very  minute,  and  its  pecu- 
liarities (see  description  of  plate)  are  better  shown  by  Fig.  81,  which 
exhibits  it  more  highly  magnified.  It  must  be  a  very  early  stage  of 
cyst  development,  for  the  cavity  is  subdivided  by  numerous  partitions, 
which  appear  as  fine  threads  in  which  are  a  few  cell-nuclei.  How 
cysts  originate  is  an  interesting  question,  but  one  which  cannot  be 
answered.  The  minute  threads  which  run  across  the  cyst,  and  which 
are,  of  course,  only  the  cut  edges  of  thin  membranes  subdividing  the 
cyst  into  numerous  chambers,  are  structurally  similar  to  the  endothe- 
lium  of  the  walls  of  capillaries.  It  is  very  common  to  find  cysts  of 
considerable  size,  notably  in  the  kidney,  which  are  divided  or  partly 
divided  by  membranes  or  membranous  shelves.  The  fact  that  the 
partitions  in  this  minute  cyst  are  so  like  endothelium  suggests  again 
the  question  of  the  influence  of  capillaries  in  the  production  of  cysts, 
and  whether  in  this  case  also  they  had  their  origin  in  the  capillaries. 

Fig.  82  represents  one  of  the  so-called  new-formed  bile-ducts. 
The  picture  is  of  tissue  near  the  capsule,  and  it  is  very  common  to 
find  the  new  ducts  in  this  region,  and  even  lying  in  the  thickened 
capsule  itself.  This  is  to  be  explained,  perhaps,  by  the  fact  that 
fibrous  tissue  is  very  apt  to  grow  in  the  neighborhood  of,  and  in  con- 
nection with,  the  capsule  of  the  liver  in  cirrhosis.  The  duct  is  seen 
to  be  composed  of  cells  like  epithelium,  which  are  arranged  in  an 
irregular  double  row,  and  it  is  forked  two  or  three  times.  It  lies  in 
fibrous  tissue,  no  liver  cells  nor  anything  that  would  enable  one  to 
recognize  that  it  is  liver  being  included.  This  forking  column  of 
cells,  which  is  a  fair  type  of  the  so-called  new  bile-ducts,  has  nothing 
in  its  appearance  that  is  like  the  ordinary  bile-ducts  in  human  liver. 
The  cells  do  not  resemble  in  the  least  the  peculiar  columnar  cells 
that  line  bile-ducts.  The  column  of  cells  in  the  picture  does,  how- 
ever, recall  to  mind  strongly  the  appearances  sometimes  presented  by 
developing  ducts  in  embryological  tissues.  In  this  resemblance  to 
developing  ducts  in  embryos  is  found  the  only  reason  why  such 
columns  of  cells,  which  are  always  very  numerous  in  hypertrophic 
cirrhosis,  are  looked  upon  as  new  bile-ducts. 

Fig.  83  presents  an  appearance  which  has  confirmed  me  in  the 


FIG.  80. — CYSTIC  DISEASE  OF  THE  LIVER,     (x  12.) 

From  a  man  of  forty-seven  years  who  died  of  cirrhosis  of  the  liver  of  the  form  some- 
times called  the  hypertrophic  cirrhosis  of  Charcot ;  the  section  was  taken  from  a  fibrous 
region  near  the  capsule.  The  central  space  is  a  cyst  large  enough  to  have  been  seen  with 
the  unaided  eye  ;  surrounding  it  is  fibrous  tissue  which  in  the  immediate  neighborhood 
of  the  cyst  is  torn  and  in  which  some  mineral  substance  (m)  was  deposited,  a  is  a  very 
minute  cyst,  represented  more  highly  magnified  in  Fig.  81. 

FIG.  81. — CYSTIC  DISEASE  OF  THE  LIVER,     (x  55-) 

The  cyst  a  from  Fig.  80,  more  highly  magnified.  It  is  surrounded  by  fibrous  tissue 
which  is  rich  in  nuclei ;  across  the  cyst-cavity  are  stretched  very  numerous  fine  threads  in 
which  there  are  a  few  nuclei.  These  threads  were  membranous  partitions  which  sub- 
divided the  cyst-cavity  into  very  many  minute  spaces. 

FIG.  82. — RETROGRESSION  OF  LIVER  TISSUE.     THE  SO-CALLED  NEW  BILE-DUCTS. 

(X  280.) 

From  the  same  case  of  Charcot' s  hypertrophic  cirrhosis  as  Fig.  80.  The  picture  repre- 
sents in  a  typical  manner  one  of  the  branching  collections  of  cells  lying  in  new-grown 
fibrous  tissue  which  it  is  usual  to  describe  as  developing  bile-ducts. 

FIG.  83. — RETROGRESSION  OF  LIVER  TISSUE,     (x  280.) 

From  the  same  tissue  as  Fig.  82.  There  is  liver  tissue  in  which  there  are  many 
cavities  exactly  like  those  described  as  a  form  of  cyst  in  Figs.  74  and  75  ;  they  are  usually 
very  numerous  in  cases  of  hypertrophic  cirrhosis,  /"is  fibrous  tissue,  d  would  probably 
be  commonly  described  as  a  developing  bile-duct.  To  the  left  it  is  composed  of  a  closely 
packed  collection  of  small  cells  which  are  arranged  in  a  double  row,  while  at  its  right-hand 
end,  where  it  is  broadest,  its  appearance  is  exactly  that  of  somewhat  degenerated  liver  cells 
with  invisible  or  very  shadowy  nuclei.  The  appearance  suggests  the  explanation  that  what 
was  once  a  trabecula  of  liver  cells  has  been  compressed  by  the  growing  fibrous  tissue  until 
it  assumed  the  condition  described  and  depicted. 


Fig.SO 


1mm 


Fig.  8 2 


Moo  mm . 

I     l     I     I    I 


THE   LIVER.  109 

opinion  I  held  before  I  ever  saw  this  particular  section,  that  the  so- 
called  new  bile-ducts  the  formation  of  which  is  the  most  pronounced 
feature  of  Charcot's  hypertrophic  cirrhosis  of  the  liver  are  not  bile- 
ducts,  and  that  the  common  explanation  of  their  presence  is  erro- 
neous. In  mammalian  embryos  the  liver  is  a  very  large  organ  de- 
veloped from  the  alimentary  canal.  At  first  there  are  ducts  which 
become  more  and  more  complex,  then  the  columns  of  liver  cells 
appear.  It  may  almost  be  said  that  the  trabeculae  of  secreting  cells 
are  developed  from  the  bile-ducts,  or,  if  this  is  not  considered  to  be 
exactly  the  case,  it  is  certainly  true  that  liver  cells  appear  after  bile- 
ducts  have  been  formed  and  in  direct  connection  with  them.  Upon 
examination,  the  theory  that  nature  forms  a  vast  number  of  new 
bile-ducts  in  hypertrophic  cirrhosis  of  the  liver,  which  is  a  process 
of  destruction,  seems  a  strange  one  and  most  unlikely.  There  is 
not  known  in  human  pathology  any  other  instance  of  such  useless 
development.  Why  should  bile-ducts  grow  in  vast  numbers  in  a 
liver  undergoing  rapid  destruction?  It  has  already  been  suggested 
by  Goodhart*  that  there  is  no  growth  of  new  ducts  in  hypertrophic 
cirrhosis,  and  he  quotes  from  others  in  support  of  this.  Fig.  83 
shows  a  column  of  cells  which  aids  to  prove  the  view  to  be  correct 
that  the  process  is  one  of  retrogression,  that  the  trabeculae  of  liver 
cells,  owing  to  the  pressure  to  which  they  are  subjected,  or  to  mere 
shrinkage  in  process  of  degeneration,  become  changed  into  columns 
of  cells  of  the  kind  which  have  been  supposed  to  be  new  bile- 
ducts.  This  particular  column  of  cells  (d,  Fig.  83)  has  at  one  end 
the  appearance  of  a  so-called  new  bile-duct,  being  composed  of  a 
double  row  of  closely  appressed  epithelial  cells,  and  at  the  other  end 
it  is  made  up  of  secreting  cells.  The  drawing  does  not,  of  course, 
show  this  so  well  as  the  object  itself  when  it  is  examined  with  the 
microscope  and  the  different  parts  are  accurately  brought  into  focus 
and  the  details  studied.  The  exhibition  of  the  transition  of  a  liver  tra- 
becula  into  a  duct,  a  thing  quite  unknown  in  healthy  liver,  does  not 
seem  susceptible  of  any  other  explanation  than  that  the  process  is  one 
of  retrogression  or  involution,  the  cells  changing  and  shrinking  to 
return  nearly  to  their  primary  embryological  state.  A  change  paral- 
lel to  this  may  occur  in  the  kidney  in  fibrosis,  a  renal  tubule  being 
compressed  until  it  looks  very  like  d  in  Fig.  83.  Such  a  condition  is 
illustrated  by  Fig.  1 16.  The  fact  that  the  squeezing  by  fibrous  growth 

*  New  Sydenham  Society,  Atlas  of  Pathology,  Fasciculus  iv. 


no  THE    ORIGIN   OF   DISEASE. 

produces  very  similar  appearances  both  in  the  liver  and  in  the  kidney 
strengthens  the  view  that  it  is  a  retrogressive  change  in  the  direction 
of  the  embryological  condition.  The  drawing  shows  also  that  the 
liver  was  full  of  holes  similar  to  those  already  described.  Such  spaces 
are  in  my  experience  invariably  present  in  cirrhosis,  and  especially 
in  hypertrophic  cirrhosis,  of  the  liver,  and  it  does  not  seem  possible 
that  they  are  only  the  result  of  ordinary  fatty  degeneration.  The 
number  of  these  spaces  is  often  very  great.  In  one  case  in  partic- 
ular, of  a  woman  who  died  with  a  liver  weighing  thirteen  pounds, 
which  was  very  hard  and  did  not  feel  or  look  in  the  least  oily,  it  was 
difficult  with  the  microscope  to  recognize  the  tissue  as  liver.  The 
appearance  was  that  of  innumerable  holes  surrounded  by  fibrous  walls, 
which  were  much  thicker  than  the  usual  envelopes  of  fat-globules ; 
only  here  and  there  after  careful  search  could  a  few  characteristic  cells 
be  found  to  betray  that  the  tissue  was  liver.  In  another  case,  of  a  boy 
of  seventeen  who  died  of  hypertrophy  of  the  heart  and  in  whom  the 
pericardial  sac  was  obliterated  by  inflammatory  adhesion,  a  chemical 
analysis  to  test  the  amount  of  fat  was  made  for  me  by  Professor  John 
Marshall.  When  dried,  the  liver  was  found  to  contain  forty-six  per 
cent,  of  oil.  In  normal  dried  liver  the  amount  of  oil  is  ten  and  one- 
half  per  cent.  This  liver  was  noted  at  the  post-mortem  examination 
to  be  "  exceedingly  enlarged,  not  greasy,  remarkably  mottled."  When 
examined  with  the  microscope,  it  seemed  to  be  a  mass  of  holes  and 
little  else.  The  amount  of  oil  as  shown  by  the  analysis  was  little 
more  than  four  times  the  normal,  while  the  microscopical  appear- 
ance of  the  tissue  was  such  as  to  make  it  seem  that  the  percentage 
must  have  been  at  least  eighty  or  ninety  if  all  the  holes  had  been 
filled  with  oil.  The  process  has  been  described  as  vacuolation,  and 
perhaps  it  is  this  form  of  degeneration  that  is  meant  by  "  cavernous 
metamorphosis,"  but  no  satisfactory  explanation  of  these  diseases  has 
been  suggested.  The  conclusion  to  which  I  am  driven  is  that  the 
commonly  accepted  theory  that  these  holes  are  all  the  result  of  fatty 
degeneration  is  inadequate  to  explain  the  disease.  It  has  already 
been  suggested  that  the  process  is  an  early  stage  of  cystic  disease. 
In  the  vast  majority  of  cases,  however,  they  never  become  sufficiently 
large  to  be  distinguishable  with  the  unaided  eye. 

Figs.  84  and  85  represent  the  appearances  of  ordinary  contracting 
cirrhosis  of  the  liver,  or,  as  it  is  often  named,  Laennec's  cirrhosis. 
The  first  of  them  is  from  the  liver  of  a  woman  of  sixty  who  died  of 
Bright's  disease  with  extensive  fibrosis  of  the  heart,  spleen,  and  kid- 


aigotfni?  1o  ij 

rfj  \  tA     .sw 
~io  anmtrli 
ii>it'jfli  •  ^m 
6rft  vi.^v 


lt   *>rft  oT 


U  l 


• 


FIG.  84. — CIRRHOSIS  OF  THE  LIVER,     (x  46.) 

From  a  woman  sixty  years  old  who  died  of  Bright's  disease.  It  is  typical  of  cirrhosis  : 
there  are  islands  of  liver  cells  surrounded  by  broad  bands  of  fibrous  tissue.  At  j  the 
fibrous  tissue  and  blood-spaces  are  greatly  increased  in  bulk,  while  the  columns  of  cells 
are  attenuated,  being  in  process  of  extinction.  The  whole  island  was  being  rapidly  ex- 
tinguished. The  capsule  is  indicated  by  f  and  g,  which  denote  respectively  the  outer 
free  surface  and  the  under  surface.  In  this  section  no  distinction  can  be  made  between 
the  capsule  and  the  fibrous  bands  extending  downward  into  the  liver,  for  they  are  identical 
in  structure  and  continuous  one  with  the  other.  Fig.  85  presents  a  striking  contrast  in 
this  respect. 

FlG.  85. — FlBROSIS   OF  THE   LlVER.       (X   48.) 

From  a  man  fifty-seven  years  old  who  died  of  Bright's  disease.  To  the  right  in  the 
drawing  (e)  dense  fibrous  tissue  bands  extend  into  the  liver  and  are  continuous  with  the 
capsule,  which  is  of  similar  structure  with  and  indistinguishable  from  the  bands.  In  this 
respect  the  appearance  is  the  same  as  in  Fig.  84.  To  the  left  in  the  drawing  the  capsule 
has  a  different  appearance,  /"is  its  upper  and^-  its  lower  surface.  Upon  it  has  grown  a 
fibromatous  deposit,  u  with  its  diverging  lines  indicates  the  thickness  of  this,  and  under- 
neath this  region  the  thickened  capsule  merges  into  the  liver  substance  so  that  there  is  no 
line  of  demarcation  between  them,  and  the  fibrous  capsule  is  evidently  growing  in  thick- 
ness at  the  expense  of  the  liver.  Under  the  fibroma  the  capsule  is  depressed,  d  is  a 
fibrous  band  extending  into  the  substance  of  the  liver.  The  columns  of  liver  cells  have 
been  made  thin  by  pressure. 


FIG.  84. 


Km.  85. 


THE   LIVER.  in 

neys,  as  well  as  of  the  liver.  There  are  islands  of  liver  surrounded 
by  broad  bands  of  fibrous  tissue ;  the  columns  of  secreting  cells  in  the 
islands  are  narrow,  are  in  process  of  destruction,  and  the  blood-spaces 
are  enlarged.  It  is  probable  that  the  true  liver  skeleton,  the  fine  but 
strong  fibrous  framework  in  which  the  columns  of  secreting  cells  are 
held,  undergoes  increase  as  a  part  of  the  general  process  of  fibrosis. 
The  persistence  of  this  framework  in  nutmeg  liver  in  portions  of  the 
organ  from  which  all  trace  of  the  secreting  cells  has  disappeared  has 
been  mentioned  (page  102).  In  the  present  case  the  thickened  capsule 
of  the  liver  is  continuous  with  the  fibrous  bands  which  ramify  among 
the  liver  islands,  and  is  of  exactly  similar  structure,  so  that  it  cannot 
be  said  where  the  one  ends  and  the  other  begins.  Fig.  85  is  from  the 
liver  of  a  man  of  fifty-seven  who  died  of  Bright's  disease.  He  had 
extreme  fibrosis  of  many  of  the  organs  and  of  the  arteries,  and  much 
calcareous  material  had  been  deposited  in  the  tissues,  organs,  and 
arteries.  The  cirrhosis  was  of  less  advanced  stage,  and  the  morbid 
fibrous  tissue,  being  of  recent  formation,  is  more  cellular  and  less 
purely  fibrous  than  in  the  first  case.  It  is  also  less  sharply  separated 
from  the  liver  substance,  the  two  merging  at  their  junction  instead 
of  showing  a  sharp  line  of  demarcation.  The  capsule  of  the  liver 
is  thickened,  and  in  a  part  of  the  tissue  represented  it  is  continuous 
with  bands  of  fibrous  tissue  which  have  penetrated  into  the  liver 
substance.  In  another  part,  the  capsule  although  decidedly  thicker 
than  natural  is  made  up  of  distinct  fibres  to  a  much  less  degree  and 
merges  into  the  liver  substance  beneath,  so  that  there  is  no  line  of 
separation,  and  at  this  place  it  shows  how  fibroid  tissue  is  growing  at 
the  expense  of  the  liver.  A  characteristic  feature  of  the  process  is 
the  growth  of  fibrous  material  upon  the  surface  of  the  capsule.  This 
is  very  common  in  the  liver,  but  even  more  so  in  the  spleen  (page  1 16). 
Such  fibrous  growths  sometimes  take  the  form  of  minute  fibromatous 
tumors,  or,  as  in  this  instance,  it  may  be  only  a  small  amount  of  loose- 
meshed  material  of  coarse  fibrous  strands  containing  scattered  cells. 
A  fibrous  growth  of  this  nature  upon  the  surface  of  the  capsule 
usually  forms  for  itself  a  depression  in  which  to  lie,'  and  such  is  the 
case  with  this  one.  The  shrinkage  of  the  fibrous  tissue  pulling  at  its 
attached  ends  draws  the  capsule  over  it  as  a  bow  is  drawn  by  the 
string,  and  thus  the  fibrous  growth  sinks  in  the  softer  substance 
beneath  it.  It  is  very  common  to  find  many  of  the  so-called  new 
bile-ducts  in  cases  of  cirrhosis  of  the  atrophic  as  well  as  the  hyper- 
trophic  form.  In  fact,  all  the  histological  features  which  have  been 


ii2  THE   ORIGIN   OF   DISEASE. 

supposed  to  be  peculiar  to  hypertrophic  cirrhosis  are  to  be  found  in 
the  contracting  form. 

Fig.  86,  which  is  from  the  liver  of  a  man  of  forty-eight  who  died 
of  dysentery,  illustrates  an  early  stage  of  hepatic  fibrosis.  Fibrous 
tissue  has  developed  in  the  midst  of  the  liver  substance,  and  the  ap- 
pearances seem  to  indicate  that  the  theory  which  was  advanced  long 
ago  that  the  liver  cells  themselves  are  converted  into  fibrous  tissue 
is  correct.  It  appears  as  if  some  of  the  secreting  cells  were  under- 
going such  a  transformation.  The  picture  shows  also  what  seems  to 
be  an  increase  of  the  fine  fibrous  framework.  The  framework  of  the 
liver  is  like  a  complicated  system  of  fine  tubes  into  the  interior  of 
which  the  liver  cells  are  packed  in  columns.  The  fact  has  already 
been  mentioned  that  this  framework  or  skeleton  is  very  persistent  and 
of  considerable  strength,  for  it  often  preserves  its  form  unchanged 
in  cases  of  nutmeg  liver  after  the  liver  cells  themselves  have  entirely 
disappeared.  It  has  been  disputed  in  the  past  whether  there  is  any 
fibrous  tissue  in  the  liver  except  that  of  Glisson's  capsule,  but  it  would 
be  impossible  for  any  one  after  examining  sections  of  nutmeg  liver 
from  which  the  secreting  cells  have  disappeared  to  doubt  that  there  is 
a  supporting  frame  to  hold  the  cells  in  their  positions,  and  that  this 
frame  is  of  different  structure  from  the  cells  themselves.  There  can 
be  no  doubt  that  the  growth  due  to  disease  of  this  fine  framework 
goes  to  form  part  of  the  masses  of  fibrous  tissue  that  are  found  in 
the  liver  in  cirrhosis,  and  it  is  probable  that  the  liver  cells  themselves 
by  some  process  of  conversion  or  of  retrogression  contribute  toward 
the  fibrous  formation.  The  question  of  the  origin  of  cirrhosis  is  an 
important  one,  and  it  is  most  likely  that  the  view  is  correct  that  the 
first  visible  sign  of  it  is  an  increase  of  the  number  of  the  nuclei  of 
Glisson's  capsule  in  the  portal  channels.  The  illustration  exemplifies 
the  fact  that  in  any  particular  disease  it  is  very  common  to  find  other 
pathological  lesions  besides  those  which  are  peculiar  to  it,  and  some- 
times in  organs  in  which  they  would  be  least  expected,  if  they  are 
carefully  sought.  In  this  case  the  patient  died  of  dysentery,  and  there 
is  every  reason  to  suppose  that  the  hepatic  fibrosis  was  of  older  date 
than  the  dysentery.  Whether  such  fibrosis  of  organs  is  harmless  or 
becomes  the  seat  of  origin  of  disease  is  a  most  important  point  in  a 
general  question  of  vast  extent.  It  is  certain,  however,  that  such 
fibroid  changes  are  sure  to  come  in  the  organs  of  all  people  if  life  is 
sufficiently  prolonged.  In  some  the  change  is  late,  and  in  others  it  is 
early.  It  is  apt  to  begin  early  in  those  who  have  suffered  with  chronic 


FIG.  86. — FIBROSIS  OF  THE  LIVER  IN  SCATTERED  SPOTS,     (x  90.) 

From  a  man  of  forty-eight  years  who  died  of  dysentery.  The  increase  of  fibrous  tissue 
is  very  plain,  and  it  is  certain  that  it  is  the  result  of  disease,  for  the  area  depicted  is  not 
near  any  portal  vein,  around  which  there  is  always  fibrous  tissue. 


FIG.  86. 


THE   LIVER.  113 

disease,  and  to  be  found  in  persons  who  have  the  appearance  of  pre- 
mature age. 

Fig.  87  represents  a  curious  form  of  disorganization  and  fibrosis  of 
the  liver.  It  is  from  a  woman  thirty  years  old  who  died  of  an  irregu- 
lar form  of  Bright's  disease  after  having  had  persistent  vomiting  for 
several  weeks.  The  natural  arrangement  of  the  liver  cells  in  columns 
is  entirely  lost.  They  lie  irregularly  scattered  each  by  itself  or  two  or 
three  together,  and  the  intervals  between  the  cells  are  filled  with  a 
fine,  almost  structureless  material.  Such  a  condition  is  difficult  to 
explain.  There  were  degeneration  of  the  heart  (Fig.  53),  two  minute 
aneurisms  in  the  aorta  (Figs.  30,  31,  and  32),  fibrosis  of  the  spleen 
and  kidneys,  and  a  peculiar  degeneration  of  the  stomach  (Fig.  103), 
besides  the  disease  of  the  liver.  It  seems  as  if  the  fibrosis  and  sub- 
inflammation  which  are  of  such  frequent  occurrence  in  old  people  and 
come  on  so  slowly  that  the  organism  has  time  to  become  accustomed 
to  them  and  acquire  the  power  to  bear  them  had  in  this  instance  come 
rapidly  in  a  woman  only  thirty  years  old, — that  old  age  had  come  upon 
her  with  such  speed  that  it  killed  her  suddenly. 

Two  notable  conditions  are  illustrated  by  Fig.  88,  which  is  from 
the  liver  of  a  man  of  twenty-seven  who  died  of  acute  cholera  morbus. 
There  are  a  number  of  spaces  within  liver  cells.  These  would  prob- 
ably be  called  by  most  pathologists  vacuoles,  but  to  say  that  such  an 
appearance  is  the  result  of  vacuolation  is  only  to  name  a  thing  which 
is  neither  described  nor  explained.  If  there  really  be  such  a  process 
as  vacuolation,  it  must  be  a  miniature  form  of  cystic  degeneration,  and 
the  appearances  here  depicted  bear  out  this  view.  The  cavities  are 
surrounded  by  distinct  walls,  as  is  usually  the  case  with  small  cysts, 
and  there  is  a  little  fine  structureless  material  lying  within  them.  The 
second  point  of  interest  illustrated  by  the  drawing  is  the  demonstra- 
tion of  other  disease  besides  lesion  of  the  intestine  in  a  case  of  acute 
cholera  morbus  of  a  duration  of  only  about  forty-eight  hours. 

In  the  liver,  as  in  all  other  parts  of  the  body,  it  is  very  common  for 
the  blood-vessels  to  be  diseased.  Those  most  commonly  affected  are 
the  branches  of  the  hepatic  artery,  the  walls  of  which  become  thick- 
ened in  every  possible  degree,  from  the  slightest  increase  of  the  intima 
to  total  closure  of  the  vessel  by  endarteritis  obliterans.  The  other 
vessels  also  are  liable  to  disease,  the  portal  veins  being  frequently 
affected,  but  in  my  experience  disease  of  the  hepatic  veins  of  such 
degree  as  to  attract  attention  is  not  very  common.  Disease,  there- 
fore, is  most  frequent  in  those  vessels  which  have  in  proportion  to  their 


ii4  THE   ORIGIN   OF   DISEASE. 

calibres  the  thickest  walls  and  are  surrounded  by  connective  tissue, 
— the  hepatic  arteries, — and  least  frequent  in  those  of  which  the  walls 
are  thinnest  and  which  are  without  connective  tissue  around  them, — 
the  hepatic  veins.  With  regard  to  blood-vessels  in  the  liver,  it  is  a 
curious  fact  that  in  cirrhosis  even  of  the  hypertrophic  form  with  great 
enlargement  there  is  apparent  paucity  of  vessels,  the  liver  being  hard, 
woody,  nodulated,  and  tough  on  section.  The  fact  was  mentioned  in 
connection  with  the  subject  of  hepatic  cirrhosis  that  what  have  been 
called  new  bile-ducts  are  often  to  be  found  in  the  capsule.  These  ducts 
are  frequently  present  in  the  thickened  capsule  of  the  liver  in  cases  of 
Bright's  disease,  and  were  found  by  me  in  a  case  of  associated  Bright's 
disease  and  phthisis,  in  which  the  degree  of  fibrosis  of  the  liver  was  so 
slight  that  no  one  would  have  said  there  was  cirrhosis  if  the  specimen 
had  not  been  examined  with  the  microscope.  The  association  of 
Bright's  disease  in  which  there  is  hepatic  fibrosis  with  consumption 
of  the  lungs  is  of  such  frequent  occurrence  that  it  makes  one  think 
there  must  be  some  relationship  between  the  diseases,  and  in  malignant 
disease  of  the  liver  the  microscopical  lesions  of  cirrhosis  are  some- 
times so  intimately  associated  with  the  new  growth  that  their  satis- 
factory separation  is  impossible,  and  the  mind  is  driven  to  the  con- 
clusion that  the  processes  are  by  no  means  so  far  apart  as  is  ordinarily 
taught.  In  tuberculosis  of  the  liver  more  than  of  any  other  organ 
giant  cells  are  apt  to  be  found  in  typical  form,  and  in  the  liver,  as  in 
other  organs,  it  is  occasionally  impossible  to  distinguish  between 
miliary  tubercles  and  miliary  abscesses.  The  secreting  cells  of  the 
liver  often  present  peculiarities  the  study  of  which  is  certain  some 
day  to  result  in  the  acquisition  of  knowledge  which  will  aid  in  the 
comprehension  of  disease  and  in  its  cure.  There  cannot  be  any  doubt 
that  the  number  of  the  secreting  cells  often  increases  in  disease  and 
that  the  liver  thus  becomes  enlarged.  One  of  the  commonest  micro- 
scopical appearances  of  the  cells  is  an  exaggerated  prominence  of 
the  nuclei,  so  that  they  produce  a  staring  effect  in  stained  sections, 
in  diseases  accompanied  by  active  inflammation  or  by  exaltation  of 
the  circulation  in  the  earlier  stages.  In  such  cases,  and  especially  in 
one  case  of  malignant  disease  within  the  portal  vessels,  I  have  seen  the 
nuclei  in  process  of  fission.  Such  cells,  if  preserved  more  perfectly  than 
can  be  done  with  pathological  tissues,  would  almost  surely  have  shown 
the  various  karyokinetic  changes.  It  has  been  said  that  cirrhosis  of 
the  liver  probably  has  its  beginning  in  an  increase  of  the  number  of 
nuclei  in  the  portal  channels ;  but  hepatic  fibrosis  at  an  early  stage 


FIG.  87. — DISARRANGEMENT  OF  THE  CELLS  OF  THE  LIVER  AND  FIBROSIS.     (X  105.) 

From  a  woman  thirty  years  old  who  died  of  Bright' s  disease,  having  had  persistent 
vomiting  for  several  weeks.  The  arrangement  of  the  cells  in  columns  has  been  destroyed  ; 
they  are  scattered  singly  and  in  disorder.  There  is  an  increase  of  fibrous  tissue. 

FIG.  88. — DEGENERATION  OF  LIVER  CELLS,     (x  220.) 

From  a  man  of  twenty-seven  years  who  died  of  acute  cholera  morbus.  e  indicates  cells 
which  have  within  them  spaces  which  are  empty  or  contain  some  amorphous  material. 
Such  spaces  are  surrounded  by  a  distinct  ring,  h  is  a  small  blood-vessel  cut  longitudinally 
and  containing  corpuscles. 


FIG.  87. 


THE   LIVER.  115 

occasionally  assumes  strange  forms,  and  the  acini  are  sometimes  sur- 
rounded by  fine  fibrous  tissue  in  such  a  way  that  the  liver  resembles 
that  of  the  pig.  Amyloid  disease  of  the  liver,  like  amyloid  disease 
of  other  organs,  has  long  remained  a  pathological  puzzle.  It  does 
seem,  however,  that  it  must  be  closely  connected  with  the  fibroid 
process,  or  even  one  of  its  forms.  The  consideration  of  disease  of 
the  liver  both  clinically  and  from  the  stand-point  of  gross  and  micro- 
scopical pathology  has  convinced  me  that  existing  classifications  are 
inadequate  and  unsatisfactory,  because  they  give  a  false  impression 
that  many  diseases  which  are  related  or  parts  of  one  process  are 
entirely  separate  from  one  another.  There  can  be  no  doubt,  for  in- 
stance, that  cirrhosis  is  only  the  result  of  inflammatory  and  cellular 
growth  of  a  character  similar  to  that  which  may  take  place  in  other 
parts  of  the  body,  and  therefore  that  whether  the  liver  is  enlarged  or 
reduced  in  size  the  disease  is  the  same  one  with  variations.  As  a 
pathological  process  it  is  often  on  the  one  hand  but  little  removed 
from  hypertrophy,  and  on  the  other  approaches  closely  to  malignancy 
or  tumor  growth.  The  relation  of  tuberculosis  to  these  diseases  is 
sometimes  very  close  and  the  lesions  are  hopelessly  entangled.  If 
all  these  diseases  were  known  to  be  merely  modifications  of  growth, 
the  pathology  of  the  liver  would  be  much  simplified,  and  it  would 
no  longer  be  necessary  to  fit  in  an  extraneous  material  cause,  as  it 
is  commonly  believed  must  be  done  in  cancer  and  tuberculosis.  It  is 
important  never  to  forget  that  morbid  fibrosis  constitutes  an  essential 
part  of  all  chronic  disease  of  the  liver,  and  at  the  same  time  that  the 
increase  of  fibrous  tissue  is  a  natural  consequence  of  age  in  the  human 
body.  To  estimate  justly  the  influence  of  the  natural  processes  of  age 
and  of  chronic  disease  is  often  very  difficult,  if  not  impossible. 


CHAPTER  VIII. 

THE    SPLEEN. 

THE  spleen  is  an  organ  of  unknown  function,  but  there  is  every 
reason  for  believing  that  it  plays  an  important  part  in  the  economy. 
It  is  certain  that  its  liability  to  disease  is  very  great,  and  that  it  is 
often  diseased  early  in  life.  As  early  as  the  fifth  or  sixth  month  the 
spleen  will  sometimes  be  found  to  be  pigmented  and  unnaturally 
fibroid,  with  thickened  capsule  and  trabeculae,  and  diseased  vessels,  in 
persons  dead  of  chronic  disease.  There  is  no  organ  which  shows  more 
certainly  the  increase  of  years,  as  in  older  persons  it  becomes  more 
dense  and  fibrous  and  the  vessels  thicken.  These  changes  due  to 
the  advance  of  years  may  be  concealed  in  persons  who  have  died  of 
diseases  which  occasion  enlargement  or  softening  of  the  spleen.  The 
most  frequent  lesion,  perhaps,  in  chronic  disease  is  thickening  of  the 
capsule.  The  spleen  capsule  is,  if  possible,  more  liable  to  disease  than 
the  capsules  of  other  organs,  and  adhesion  to  surrounding  parts  is 
of  very  frequent  occurrence. 

Fig.  89  is  from  the  spleen  of  a  man  of  fifty-seven  who  died  of 
Bright's  disease,  and  it  represents  thickening  of  the  capsule  in  an 
extreme  degree,  but  in  a  form  that  is  very  common.  The  natural 
capsule  remains  apparently  unchanged,  and  upon  its  outer  surface  has 
been  developed  a  layer  of  coarse  fibrous  tissue  of  very  varying  thick- 
ness. The  effect  has  been  to  force  the  capsule  downward  in  some 
places  into  the  splenic  pulp.  The  fibrous  tissue  in  this  case  has  de- 
veloped separately  and  constitutes  a  tumor  grown  upon  the  capsule. 
The  two  layers  are  distinctly  shown  by  the  drawing. 

Fig.  90  shows  a  form  of  fibrous  growth  which  is  of  frequent  occur- 
rence. It  is  a  true  fibroma,  a  tumor  developed  upon  the  surface  of 
the  capsule.  These  growths  are  in  my  experience  very  common  in 
persons  past  middle  life  who  have  died  of  chronic  disease,  and  they 
present  themselves  as  minute  seed-like  protuberances  upon  the  surface 
of  the  organ.  Such  a  growth  I  once  found  as  early  as  at  ten  years, 
and  the  spleen  was  fibroid  and  the  vessels  thickened.  The  patient 
died  of  chronic  disease  of  the  heart.  They  are  white  and  opaque  in 
most  instances,  the  capsule  is  generally  thickened  and  whiter  than 
116 


FIG.  89. — FIBROMA  OF  THE  SPLEEN,     (x  "•) 

From  a  man  of  fifty-seven  years  who  died  of  Bright' s  disease.  The  true  capsule  is  seen 
as  a  membrane  of  even  thickness,  upon  the  upper  surface  of  which  is  the  new-grown 
fibroid  tissue  constituting  a  layer  of  very  varying  thickness.  The  splenic  pulp  is  below. 

FIG.  90.— SMALL  FIBROMA  OF  THE  SPLEEN,     (x  n.) 

From  a  man  of  fifty-one  years  who  died  of  perihepatic  abscess.  The  capsule  is  of  nearly 
even  thickness,  and  the  fibrous  prolongations  from  it  into  the  splenic  pulp  constituting  the 
trabeculse  are  shown.  The  fibroma  is  set  upon  the  capsule  and  sinks  it  into  the  spleen 
pulp  :  it  may  be  compared  to  a  bow  and  its  string,  the  curved  lines  of  the  capsule  under- 
neath being  the  bow,  and  the  strands  oi  the  fibroma  the  string. 


1mm. 


FIG.  90. 


FIG.  91. — FIBROID  SPLEEN,     (x  n.) 

From  a  woman  of  sixty  years  who  died  of  Bright' s  disease.  Through  the  portion  of 
spleen  depicted,  from  top  to  bottom  there  passes  a  broad  band  of  fibrous  tissue,  a  marks 
its  boundary  on  the  left,  and  b  on  the  right.  The  boundaries  are  quite  sharply  marked,  and 
in  the  band  itself  there  is  nothing  remaining  which  is  like  ordinary  spleen  tissue.  Above, 
the  band  widens  so  as  to  be  somewhat  wedge-shaped,  with  the  base  of  the  wedge  upward 
and  against  the  capsule,  c  to  d  is  fibroma  which  has  grown  upon  the  capsule  ;  d  to  e  is 
the  capsule.  Both  the  fibroma  and  the  capsule  are  depressed  at  the  centre,  and  they  are 
thrown  into  two  folds.  In  the  depressions  caused  by  the  folds  there  is  fibrous  tissue  which 
is  less  dense  than  most  of  the  fibroma.  This  was  recent  growth,  and  in  this  manner,  partly 
at  least,  it  must  have  increased.  In  all  parts  of  the  portion  of  spleen  depicted  the 
fibrous  tissue  is  increased,  the  trabeculae  are  very  heavy,  and  the  vessels  are  thick- walled. 

FlG.  92. — FlBROSIS    OF   THE   SPLEEN.       (X   22O. ) 

From  a  negro  woman  about  seventy  years  old  who  died  of  fibrosis  of  the  heart,  lungs, 
liver,  spleen,  and  kidneys.  Above  is  a  portion  of  the  spleen  capsule.  Instead  of  the 
splenic  pulp's  consisting  almost  entirely  of  a  mass  of  lymphoid  cells,  they  are  sparse  and 
scattered  and  there  are  many  threads  of  fibrous  tissue.  The  general  effect  is  that  there 
is  not  merely  a  relative  increase  of  fibrous  tissue  produced  by  the  decreased  number  of  the 
lymphoid  cells,  but  that  the  amount  of  the  fibrous  elements  is  absolutely  increased.  The 
paucity  of  lymphoid  cells  is  very  striking. 


FIG.  91. 


Fie.  92. 


THE   SPLEEN.  117 

natural,  and  the  spleen  itself  is  more  or  less  fibroid.  Such  fibroma- 
tous  tumors  are  often  present  in  considerable  numbers.  They  con- 
stitute another  evidence  of  the  tendency  that  exists  in  older  people 
and  in  those  suffering  with  chronic  disease  to  an  unnatural  growth 
of  fibrous  tissue,  a  tendency  that  has  no  existence  in  healthy  persons 
in  early  life,  when  the  tissues  and  organs  are  all  soft  and  pliable. 

Fig.  91  is  from  the  spleen  of  a  woman  of  sixty  who  died  of  Bright's 
disease,  and  who  had  also  extreme  fibrosis  of  the  heart,  lungs,  and 
liver.  It  illustrates  splenic  fibrosis  of  the  most  extreme  form.  This 
spleen  was  rather  smaller  than  natural,  the  capsule  was  very  white 
and  irregularly  thickened,  and  on  section  the  pulp  was  hard  and 
fibroid.  The  drawing  shows  that  there  was  no  natural  spleen  tissue 
left ;  there  are  thickened  vessels,  trabeculae  cut  in  various  directions, 
and  fibrous  tissue.  Through  the  centre  of  the  portion  of  spleen  de- 
picted (see  description  of  Fig.  91)  there  runs  a  morbid  fibrous  band 
from  which  all  trace  of  spleen  tissue  has  disappeared.  Upon  the 
capsule  there  has  grown  a  layer  of  coarse  and  puckered  fibrous 
tissue,  which  in  most  places  is  quite  separate  from  the  true  capsule 
beneath,  although  in  one  place  the  two  are  somewhat  run  together. 
Fibrosis  of  the  spleen  of  some  degree  is  an  almost  invariable  accom- 
paniment of  age  and  chronic  disease.  In  combined  Bright's  disease 
and  phthisis  the  spleen  is  generally  fibroid,  and  in  a  case  of  cerebral 
apoplexy  I  was  struck  by  the  condition  of  the  splenic  blood-vessels, 
many  of  the  minute  arterioles  being  almost  closed  by  obliterative  en- 
darteritis.  The  disease-process  which  occasioned  the  cerebral  hemor- 
rhage did  not  confine  itself  to  the  brain.  Ordinarily  when  the  splenic 
vessels  become  thickened  from  disease  they  assume  a  different  ap- 
pearance from  that  of  diseased  vessels  in  other  tissues  and  organs. 
They  lose  almost  all  differentiation  into  coats,  and  appear  as  tubes 
of  nearly  homogeneous  fibrous  tissue  with  very  few  nuclei.  In  the 
natural  condition  of  the  spleen  minute  arteries  lie  in  the  trabeculae, 
and  when  diseased  they  assume  an  appearance  almost  identical  with 
that  of  the  fibrous  tissue  forming  the  trabeculae :  so  that  it  is  often  im- 
possible to  determine  how  much  of  the  fibrous  tissue  belongs  to  the 
trabeculae  and  how  much  to  the  vessel.  The  effect  produced  in  sec- 
tion is  of  a  fibrous  column  solid  except  for  the  opening  of  the  vessel 
in  its  centre,  and  this  is  often  very  small. 

Fig.  92  is  from  a  portion  of  the  spleen  of  a  negro  woman  of  about 
seventy  who  died  of  Bright's  disease  with  fibrosis  of  the  heart,  lungs, 
liver,  spleen,  and  kidneys.  The  spleen  was  small  and  very  hard,  and 


n8  THE   ORIGIN   OF   DISEASE. 

there  were  thick  scars  on  the  capsule.  It  illustrates  a  curious  phase 
of  splenic  fibrosis.  Although  this  spleen  was  noticed  at  the  post- 
mortem examination  to  be  very  hard,  its  microscopical  appearance 
would  lead  one  to  suppose  that  it  was  soft.  The  drawing  repre- 
sents a  tissue  made  up  of  fine  and  delicate  fibres  and  a  few  scattered 
leucocytes.  Healthy  spleen  as  seen  in  section  with  the  microscope 
is  composed  of  masses  of  leucocytes  so  thick  that  the  reticulum  is 
almost  entirely  concealed,  and  therefore  the  paucity  of  leucocytes 
is  the  most  striking  feature  of  the  picture.  It  is  not  likely  that  the 
tissue  would  be  recognized  as  spleen,  so  greatly  is  it  changed.  The 
fact  that  the  organ  was  very  hard  proves  that  there  was  an  abso- 
lute increase  of  fibrous  tissue.  The  woman  had  been  exceedingly 
feeble  for  a  number  of  years,  and  yet  she  had  never  had  any  very 
decided  attacks  of  illness :  so  that  her  death  might  almost  be  said  to 
have  been  from  old  age,  so  gradual  was  the  progress  of  the  changes 
in  the  organs  which  were  found  after  death.  The  microscopical  ap- 
pearance of  the  spleen  tallies  well  with  the  life-history  and  the  post- 
mortem conditions  :  it  looks  old  and  incapable.  The  increased  fibrous 
framework  and  the  few  leucocytes,  when  considered  in  comparison 
with  the  dense  and  solid  structure  of  healthy  spleen,  remind  one  of 
the  difference  between  wood  which  is  old  and  rotten  and  that  which 
is  young. 

Fig.  93,  which  is  from  the  spleen  of  a  woman  of  forty  who  died  of 
heart  disease,  illustrates  a  curious  effect  of  disease.  The  spleen  has 
been  folded  in  such  a  manner  as  to  bring  two  surfaces  of  the  capsule 
nearly  into  contact.  This  result  must  have  been  produced  while  the 
organ  was  being  reduced  in  size  after  having  been  swollen.  The  re- 
duction in  size  not  going  on  at  the  same  rate  throughout  the  organ, 
it  is  easy  to  conceive  how  it  might  have  been  folded  to  produce  the 
effect  which  is  depicted.  A  notable  feature  is  that  at  several  points 
the  contiguous  surfaces  of  the  capsule  have  been  bound  together  by 
inflammatory  adhesions.  The  capsule  is  much  thickened.  To  recog- 
nize the  details  of  structure  greater  amplification  is  required.  When 
this  is  used,  it  is  seen  that  the  adhesion  bands  are  structurally  in  many 
respects  similar  to  the  thickened  capsule.  Both  the  thick  capsule  and 
the  adhesion  bands  contain  blood-vessels  and  unnatural-looking  cells 
of  character  similar  to  those  which  have  been  described  as  composing 
part  of  the  new  tissue  which  grows  within  blood-vessels.  Such  a  fold- 
ing as  this  is  probably  not  in  itself  a  thing  of  much  consequence  except 
so  far  as  it  might  have  been  a  centre  from  which  inflammation  could 


FIG.  93.— A  FOLDED  SPLEEN,     (x  "•) 

From  a  woman  of  forty  years  who  died  of  heart  disease.  The  organ  had  been  bent 
over  so  as  to  bring  two  surfaces  of  the  capsule  nearly  into  contact,  i  is  the  capsule  ;  its 
two  surfaces,  where  contiguous  in  the  fold,  have  become  adherent  by  four  bands,  in  the 
uppermost  one  of  which  can  be  seen  a  blood-vessel  (v}. 


FIG.  93. 


FIG.  94. — CYSTIC  SPLEEN.     (X  50.) 

From  a  man  forty-eight  years  old  who  died  of  heart  disease  and  pulmonary  fibrosis. 
The  membranes  separating  the  cysts  are  in  places  distinctly  fibrous.  The  arteries  are 
thickened. 


FIG.  94- 


THE   SPLEEN.  119 

start  Similar  folding  and  adhesions  occur  in  the  liver,  but  they  are 
apt  to  be  less  deep,  for  the  liver  is  very  hard,  while  the  spleen  is  a  soft 
organ. 

In  the  chapters  on  the  heart  and  liver  it  has  been  shown  that  cysts 
are  found  in  the  heart,  and  that  they  are  probably  less  rare  in  the 
liver  than  is  commonly  believed.  It  was  suggested  that  they  may 
originate  in  the  capillaries  in  the  liver,  and  not,  as  is  generally  taught, 
in  the  bile-ducts,  and  it  was  pointed  out  that  in  the  heart  there  are  no 
pre-existing  ducts  or  cavities  in  which  true  cysts  could  arise  except 
the  blood-vessels  and  lymphatics.  The  same  obtains  in  regard  to  the 
spleen :  there  are  no  ducts  or  cavities  for  true  cysts  to  arise  in  except 
the  blood-vessels  and  lymphatics,  and,  as  disease  and  dilatations  of 
blood-vessels  are  well  known  to  be  common,  while  comparatively  little 
is  known  of  disease  of  lymphatics,  it  would  seem  much  more  likely 
that  a  cyst  in  the  spleen  had  had  its  origin  in  a  blood-vessel  than 
in  a  lymphatic.  Cavities  which  can  be  described  only  as  cysts  are 
not  rare  in  the  spleen.  Fig.  94  represents  such  cysts  in  the  spleen 
of  a  man  forty-eight  years  old  who  died  of  hypertrophy  of  the  heart 
and  pulmonary  fibrosis.  The  largest  of  the  cavities  is  but  little  more 
than  two-thirds  of  a  millimetre  across  in  its  longest  diameter,  while 
others  are  only  a  fraction  of  this  size.  They  are  all  so  minute  that  it 
is  unlikely  they  would  have  been  seen  with  the  unaided  eye.  The 
cyst-walls  in  this  instance  are  mostly  fibrous,  and  in  places  there  are 
distinct  fibrous  threads  separating  two  cavities.  As  a  general  thing, 
cysts  of  small  size  have  more  distinct  walls  than  the  larger  ones.  It 
seems  as  if  the  stretching  consequent  upon  progressive  enlargement 
breaks  through  the  walls,  so  that  the  cysts  finally  are  directly  sur- 
rounded by  the  tissue  of  the  organ. 

Figs.  95,  96,  97,  and  98  represent  cysts  in  the  spleen  of  an  elderly 
man  who  was  killed  by  illuminating-gas  poisoning,  and  who  it  was 
found  after  death  had  been  suffering  with  pulmonary  phthisis  and 
Bright's  disease.  The  patient  went  with  a  woman  to  a  room  in  a 
hotel,  where  they  must  have  blown  out  the  gas,  for  in  the  morning 
both  were  found  insensible  and  the  room  was  full  of  gas.  The  woman 
recovered  and  walked  out  of  the  hospital  within  twenty-four  hours 
after  her  admission,  but  the  man  never  regained  consciousness,  and  in 
a  few  days  the  lungs  became  congested  and  he  died.  It  is  interesting 
that  the  inhalation  of  an  amount  of  gas  that  had  no  serious  effect  upon 
a  woman  who  was  presumably  in  good  health  should  have  caused  the 
death  of  a  man  who  had  phthisis  and  Bright's  disease.  The  extensive 


120  THE   ORIGIN   OF   DISEASE. 

chronic  disease  with  which  he  was  suffering  had  probably  been  of 
latent  character,  so  that  he  did  not  himself  know  that  he  was  ill.  The 
case  affords  an  illustration  of  the  fact  which  has  been  so  much  dwelt 
upon,  that  acute  attacks  of  illness  are  often  very  much  affected  in  their 
results  by  pre-existing  chronic  disease,  and  that  chronic  disease  may 
be  so  latent  as  to  give  no  sign  of  its  existence.  The  cysts  were  of 
such  size  that  they  were  easily  seen  with  the  unaided  eye,  and  they 
present  a  number  of  points  of  interest.  The  accidental  discovery  of 
these  small  cysts  in  the  spleen  of  a  patient  who  died  of  pulmonary 
phthisis  and  Bright's  disease  and  had  also  cystic  kidneys  would  seem 
to  point  toward  some  relation  of  the  diseases  to  one  another.  It  is 
not  likely  that  the  existence  of  cysts  in  the  kidneys  and  spleen  in  the 
same  case  was  a  mere  coincidence,  but  probably  they  were  due  in 
both  organs  to  a  single  cause.  It  is  remarkable  how  very  commonly 
fibroid  and  cystic  disease  are  associated  in  persons  of  advanced  years, 
and  that  some  of  the  forms  of  pulmonary  phthisis  which  are  common 
in  advanced  life  are  found  to  exist  in  the  same  connection.  The 
occurrence  of  cysts  in  the  spleen  is  not  considered  to  be  common. 
The  cysts  illustrated  were  seen  when  cut  to  be  filled  with  a  soft,  solid 
substance,  which  the  drawing  shows  to  be  composed  of  granular  mate- 
rial intermingled  with  cells  of  a  character  unusual  in  the  spleen.  The 
cells  are  large  and  granular,  resembling  exudate  cells,  and  are  in  all 
stages  of  destruction.  It  is  impossible  to  know  from  what  portion 
of  the  splenic  tissue  such  cells  could  have  been  derived,  for  they  are 
unlike  any  of  its  normal  cells.  A  striking  characteristic  of  these 
cysts  is  that  they  all  have  strongly  differentiated  walls,  in  this  respect 
differing  from  large  splenic  cysts,  which,  as  will  be  presently  shown, 
often  are  simply  cavities  surrounded  by  splenic  tissue.  The  walls  are 
formed  of  bead-like  cells  which,  as  is  the  case  with  the  large  exudate 
cells,  are  entirely  unlike  any  cells  seen  in  normal  spleen. 

Figs.  99  and  100  illustrate  cystic  degeneration  of  the  spleen  of  great 
degree.  The  case  was  one  of  cystic  disease  of  the  heart,  spleen,  liver, 
and  kidneys  in  a  man  seventy-seven  years  old,  and  a  report  of  it  has 
been  published.*  Illustrations  showing  the  characteristics  of  the  cysts 
of  the  heart  and  liver  have  already  been  described.  The  cavities  in 
the  spleen  were  very  numerous,  there  was  great  increase  of  the  fibroid 
tissue,  and  the  blood-vessels  were  very  much  diseased  and  thickened. 
The  cysts  have  in  places  distinct  fibrous  walls,  but  are  generally  sur- 
rounded directly  by  the  splenic  tissue.  It  is  usually  the  smaller  ones 

*  Journal  of  Anatomy  and  Physiology,  vol.  xxvii.  p.  454. 


at   hfU 


a  .rrjjr; 


.31  i 


FIG.  95. — CYSTIC  SPLEEN,     (x  n.) 

From  an  elderly  man  who  died  of  illuminating-gas  poisoning  and  who  was  found  to 
have  pulmonary  tuberculosis  and  Bright' s  disease,  c  is  the  capsule  of  the  spleen.  Be- 
neath it  are  numerous  irregularly  shaped  cysts  containing  a  good  deal  of  solid  material. 
The  cavities  all  have  distinct  walls,  x  is  the  cyst  represented  more  highly  magnified  in 
Fig.  96. 

FIG.  96. — CYSTIC  SPLEEN,     (x  44.) 

The  cyst  x  in  Fig.  95,  more  highly  magnified.  The  material  within  the  cavity  is  com- 
posed of  granular  debris  and  many  large  exudate  cells,  b  is  the  upper  end  of  a  smaller 
cavity  which  also  contains  some  granular  substance.  The  walls  of  both  the  cavities  are 
fibrous,  and  there  is  at  most  places  a  lining  membrane  containing  ovoid  bead-like  cells. 
The  enlargement  is  not  sufficient  to  make  these  cells  very  distinct ;  they  can  be  better 
studied  in  Figs.  97  and  98.  a  denotes  the  area  represented  more  highly  magnified  in 
Fig.  97  ;  b,  the  area  represented  more  highly  magnified  in  Fig.  98. 

FIG.  97. — CYSTIC  SPLEEN,     (x  280.) 

The  area  a  in  Fig.  96,  more  highly  magnified.  The  line  r  to  s  corresponds  with  the 
line  extending  from  a  into  the  cavity  of  the  cyst  in  Fig.  96.  e  indicates  the  exudate 
cells ;  some  of  them  have  a  distinct  external  wall  with  sharply  defined  nucleus  and 
granular  contents,  others  are  in  various  stages  of  destruction,  the  nuclei  melting  down, 
the  walls  gone,  and  the  cells  running  together  to  become  mere  masses  of  structureless 
granular  debris.  w  is  the  wall  dividing  the  large  cyst  from  the  small  one  ;  its  central 
portion  consists  of  fibrous  tissue,  and  upon  each  side  are  the  membranes  containing  ovoid 
bead-like  cells  (c)  which  formed  the  lining  of  the  larger  and  smaller  cysts,  z  is  a  portion 
of  the  wall  to  the  right  of  the  smaller  cyst. 

FIG.  98. — CYSTIC  SPLEEN,     (x  280.) 

A  free-hand  sketch  of  the  upper  portion  of  the  smaller  cyst  in  Fig.  96  and  indicated 
by  b.  Drawn  with  the  same  amplification  as  Fig.  97  and  to  correspond  with  it  in  size. 
In  the  lower  part  of  the  picture  the  cyst- walls  have  been  cut  sharply  across,  and  the  bead- 
like  oval  cells  in  the  lining  membrane  are  distinct,  while  in  the  upper  portion  the  plane 
of  section  has  been  somewhat  sloping,  cutting  the  cells  across  in  such  a  manner  that  they 
look  like  somewhat  disarranged  epithelium. 


Fio.95 


x 


'IP.  96 


Fig.  98 


- 


FIG.  99. — CYSTIC  SPLEEN.     (X  6.) 

From  a  man  of  seventy-seven  years  who  had  also  cystic  disease  of  the  heart,  liver,  and 
kidneys,  c  is  the  capsule.  The  cysts  are  of  various  sizes,  and  some  have  a  fibrous  cyst- 
wall  and  others  are  without  any.  d  is  a  fibrous  cyst-wall,  e  denotes  a  portion  of  the 
section  torn  in  preparation  (not  a  cyst),  k  is  the  area  shown  more  highly  magnified  in 
Fig.  100. 

FIG.  loo. — CYSTIC  SPLEEN,     (x  50.) 

The  area  k  in  Fig.  99,  more  highly  magnified.  /  is  a  trabecula.  There  are  several 
cysts  included  :  some  contain  structureless  solid  material,  others  are  empty.  Around  the 
cysts  there  is  no  fibrous  wall,  the  spleen-pulp  constituting  their  boundaries.  /  is  fibrous 
tissue  which  was  broken  in  process  of  preparation  :  it  was  part  of  a  cyst-wall.  Two 
minute  thickened  vessels  are  included. 


FIG.  99. 


THE   SPLEEN.  121 

that  have  fibrous  walls,  while  the  larger  ones  lie  directly  in  the  splenic 
pulp.  It  is  notable  that  cysts  were  found  in  four  of  the  greatest 
organs  of  the  same  body,  and  it  is  probable  that  they  had  the  same 
cause  and  the  same  mode  of  origin  in  all  four.  It  is  much  the  custom 
in  medicine  at  the  present  time  to  attribute  disease  to  infection,  espe- 
cially diseases  which  are  obscure  and  difficult  to  understand,  and  when 
similar  lesions  occur  in  many  different  organs  to  attribute  them  to 
metastasis,  which  is  but  another  way  of  expressing  an  extension  of 
disease  by  infection  from  one  organ  to  another.  In  this  case  of  cystic 
degeneration  certainly  no  process  of  infection  was  at  work,  but  a 
common  cause  or  tendency  produced  a  similar  effect  in  different  and 
unrelated  parts.  The  occurrence  of  cystic  disease  of  four  great 
organs  is  just  as  remarkable  as  that  of  cancer  of  several  organs  which 
is  so  common,  and  I  have  never  been  able  to  see  that  there  is  any 
greater  reason  for  the  assumption  of  the  existence  of  an  infective  cause 
for  the  metastasis  of  cancer  than  there  would  be  for  a  similar  assump- 
tion in  regard  to  the  causation  of  the  cysts. 

Figs.  101  and  102  show  a  condition  of  the  spleen  which  in  my  ex- 
perience is  very  common.  The  section  is  from  the  spleen  of  a  youth 
of  seventeen  who  died  of  hypertrophy  of  the  heart.  Much  of  the 
tissue  represented  is  natural,  except  that  there  is  slight  increase  of 
fibrous  tissue  and  the  blood-vessels  are  very  much  thickened  from 
obliterative  arteritis,  but  part  of  it  is  full  of  minute  holes.  The  con- 
trast of  appearance  between  that  portion  which  contains  the  holes 
and  the  solid  part  is  best  seen  in  the  low-power  drawing,  while  the 
details  of  structure  can  be  distinguished  only  in  the  one  drawn  with 
greater  amplification.  Cavities  such  as  these  have  been  described  as 
pulp-sinuses,*  and  the  condition  named  active  hyperaemia  of  the 
spleen,  but  the  cavities  are  represented  as  being  filled  with  blood, 
while  in  my  illustration  it  is  seen  that  there  is  nothing  like  blood  in 
any  of  them.  Even  if  the  cavities  were  filled  with  blood  it  would  not 
prove  that  they  were  natural  blood-spaces,  for  it  has  already  been 
shown  in  connection  with  the  liver  (page  104)  that  in  cases  of  conges- 
tion all  the  cavities  and  even  the  solid  tissues  become  filled  with  red 
corpuscles,  the  blood  forcing  its  way  out  of  its  natural  channels  and 
filling  places  in  which  it  does  not  properly  belong.  Some  of  these 
cavities  are  more  than  one-half  of  a  millimetre  across,  and  they  do 
not  resemble  any  other  known  vascular  space.  The  cells  with  which 
their  lining  is  studded  are  more  like  those  seen  in  cyst-walls  than 

*  Practical  Pathology,  third  edition,  by  G.  Sims  Woodhead,  p.  417. 


122  THE   ORIGIN   OF   DISEASE. 

anything  else.  Such  cavities  are  certainly  not  natural  in  the  spleen, 
and  to  call  them  pulp-sinuses  and  suppose  them  to  be  blood-channels 
is  an  unsatisfactory  way  of  explaining  their  existence.  To  assume  that 
they  are  an  early  stage  of  cyst  development  would  be  premature,  and 
yet  the  thought  that  such  may  be  the  case  cannot  be  escaped.  The 
case  from  which  the  illustration  was  taken  was  a  youth  who  died  of 
chronic  disease,  and  chronic  disease  always  makes  those  who  suffer 
with  it  old  before  their  time.  In  my  experience,  one  of  the  com- 
monest appearances  in  the  spleen  of  old  persons  and  of  those  who 
have  died  of  chronic  disease  is  the  presence  of  such  cavities  as  have 
been  shown,  and  I  believe  it  to  be  a  disease  which  is  not  satisfactorily 
explained  as  acute  hyperaemia  of  the  spleen.  Study  of  the  spleen  is 
to  a  certain  extent  unsatisfactory,  as  its  function  is  unknown.  So  far 
as  can  be  at  present  understood,  it  is  seldom  the  site  of  primary  dis- 
ease, but,  on  the  other  hand,  the  morbid  changes  which  occur  in  it 
are  worthy  of  careful  study,  for  no  organ  is  more  liable  to  change 
with  the  advance  of  years,  and  it  always  bears  its  part  in  the  exten- 
sive diffuse  lesions  which  accompany  chronic  disease,  being  especially 
liable  to  fibrosis,  disease  of  its  vessels  and  capsule,  and  adhesion  to 
surrounding  parts. 


FIG.  101. — SMALL  CAVITIES  IN  THE  SPLEEN.     (X  50-) 

From  a  youth  of  seventeen  years  who  died  of  hypertrophy  of  the  heart  with  pericardia! 
adhesion,  o  indicates  the  cavities,  which  are  of  varying  sizes  and  shapes.  The  portion  of 
spleen  containing  the  cavities  shades  off  into  tissue  which  is  natural  in  appearance,  except 
that  the  vessels  are  thickened.  The  area  o  is  represented  more  highly  magnified  in  Fig. 

102. 

FIG.  102. — SMALL  CAVITIES  IN  THE  SPLEEN,     (x  220.) 

An  enlarged  view  of  the  area  o  in  Fig.  101.  The  cavities  are  lined  with  cells  which  it 
is  difficult  to  classify.  They  are  too  large  to  be  leucocytes,  and  have  not  their  appearances, 
and  yet  they  cannot  be  called  epithelial  cells. 


Fie.  101. 


FIG.  102. 


CHAPTER    IX. 

THE   STOMACH. 

THE  stomach  is  an  unsatisfactory  organ  in  which  to  study  minute 
pathological  changes.  When  the  lesions  are  gross,  as  is  sometimes 
the  case  in  cancer  or  ulcer,  they  are  easily  recognized,  but  even  ulcera- 
tion  of  the  stomach  is  not  always  easy  to  understand,  for  it  is  impos- 
sible sometimes  to  know  how  much  of  the  destruction  which  is  seen 
was  effected  post  mortem.  A  gastric  ulcer  itself  may  rapidly  change 
after  death.  This  difficulty  of  the  study  of  disease  of  the  stomach  is 
true  both  of  investigations  made  directly  and  of  those  with  the  micro- 
scope. The  microscopical  appearances  of  sections  of  human  stomach 
taken  from  persons  who  have  died  of  disease  are  so  different  from 
what  we  are  taught  by  histologists  is  natural,  that  it  is  one  of  the 
greatest  difficulties  of  the  pathologist  to  decide  to  what  extent  the 
changes  which  he  sees  are  the  result  of  disease,  or  if  they  occurred 
post  mortem.  The  histologist  takes  one  of  the  lower  animals,  and, 
after  killing  it  by  some  very  rapid  method,  removes  the  stomach  and 
places  it  in  a  preservative  fluid  before  there  is  time  for  post-mortem 
changes  to  occur.  It  is  curious  that  of  all  the  human  stomachs 
I  have  ever  examined  not  one  was  lined  with  columnar  epithelium, 
as  we  are  taught  is  normal.  The  columnar  cells  are  still  found  in 
the  follicles,  but  from  the  lining  surface  they  have  disappeared.  The 
rapidity  of  the  post-mortem  changes  is  attributed  to  direct  macer- 
ation and  destruction  by  the  gastric  juice.  An  almost  exact  parallel 
to  this  is  found  in  the  pancreas.  Sections  of  human  pancreas  bear 
little  resemblance  to  the  normal,  the  characteristics  of  which  have 
been  learned  from  the  tissue  of  lower  animals.  The  cells  are  in  such 
a  condition  that  they  cannot  be  satisfactorily  studied,  and  this  makes 
the  preceding  statement  in  regard  to  the  stomach  true  also  of  the 
pancreas, — that  study  of  its  minute  pathological  conditions  does  not 
yield  satisfactory  results.  Although  the  preservation  of  the  cells  in 
perfect  condition  is  impossible,  on  the  other  hand  there  can  be  no 
doubt  that  consistent  microscopical  study  of  the  stomach  and  pan- 
creas and  of  the  intestines  carried  out  in  all  sorts  of  cases,  whether  or 
not  there  was  any  disease  that  could  be  recognized  by  the  naked  eye, 

123 


124  THE   ORIGIN   OF   DISEASE. 

would  yield  very  valuable  results.  In  this  way  it  would  be  possible 
for  an  individual  investigator  to  acquire  a  personal  experience  of  the 
appearances  of  the  stomach  which  would  enable  him  to  recognize 
slight  pathological  lesions,  instead  of  those  only  which  are  gross  and 
therefore  very  obvious.  A  difficulty  which  always  confronts  the 
pathological  histologist  is  to  decide  in  the  human  tissues  subjected 
to  his  examination  how  closely  he  may  demand  of  them  an  approxi- 
mation in  appearance  to  accepted  histological  standards.  An  interval 
always  elapses  after  death  before  an  examination  of  a  human  body 
can  be  made,  and  in  persons  who  have  died  of  diseases  like  typhoid 
fever,  in  which  the  temperature  is  high,  the  tissues  are  softened  and 
unsatisfactory  to  study  so  far  as  concerns  the  cells.  It  is  almost  cer- 
tain that  this  soft  condition  of  the  tissues  and  the  ill-defined  state 
of  the  cells  existed  during  life  in  such  diseases,  and  are  not  purely 
post-mortem  changes.  During  the  course  of  diseases  of  this  class, 
and  especially  during  the  later  stages,  when  death  approaches,  the 
condition  of  relaxation  is  extreme,  the  tissues  tending  to  slough,  as 
is  shown  by  the  frequency  of  bed-sores.  It  does  not  seem,  therefore, 
unreasonable  to  believe  that  the  tissues  have  degenerated  and  the 
cells  have  lost  their  activity  before  death.  It  is  as  though  the  body 
had  begun  to  decay  before  death  occurred. 

It  is  unusual  to  find  a  layer  of  pavement  cells  upon  the  capsules 
of  the  abdominal  organs,  or  upon  the  surfaces  of  the  lungs,  or  upon 
the  lining  of  the  pleural  cavities.  The  capsules  are  usually  simply 
fibrous  membranes  without  any  trace  of  a  differentiated  pavement 
layer  upon  the  surface.  The  endothelial  layer  of  the  pleura  and 
of  the  peritoneum  which  is  so  minutely  described  by  histologists  has 
almost  no  existence  in  human  pathology.  In  consequence  of  disease 
or  of  post-mortem  change,  no  trace  of  it  is  found.  In  old  persons 
and  in  those  who  have  suffered  with  chronic  disease  it  is  so  usual  to 
find  the  capsules  of  the  abdominal  organs  and  the  pleural  covering  of 
the  lungs  thickened  that  one  is  tempted  to  think  the  endothelial  layer 
disappears  as  life  goes  on  and  the  coverings  of  organs  become  fibrous 
and  thick. 

The  stomach  calls  for  more  frequent  study,  and  such  study  will 
yield  useful  information.  Fig.  103  represents  a  section  of  the  stomach 
of  a  woman  of  thirty  who  died  of  Bright's  disease  after  persistent 
vomiting  lasting  several  weeks.  The  case  has  already  been  mentioned 
and  illustrations  given  of  the  appearances  of  several  organs, — heart 
muscular  fibres,  minute  aortic  aneurisms,  and  liver  (Figs.  30,  31,  32, 


FIG.  103. — DEGENERATION  OF  THE  STOMACH,     (x  n.) 

From  a  woman  aged  thirty  years  who  died  of  Bright' s  disease,  having  had  persistent 
vomiting  for  many  weeks.  The  mucous  coat  is  not  normal ;  it  is  of  uneven  thickness,  and 
the  follicles  cannot  be  recognized,  to  such  an  extent  have  they  melted  together.  Epithelial 
cells  are  not  distinguishable.  The  submucous  coat  is  a  little  thick  and  loose-meshed,  but 
neither  it  nor  the  muscular  coat  presents  any  definite  appearances  of  disease. 


FIG.  103. 


THE   STOMACH.  125 

53,  and  87).  The  appearance  of  the  stomach  is  unusual,  and  has  been 
produced  by  disease.  The  follicles  and  cells  have  lost  their  distinct- 
ness, having  run  together  to  form  a  layer  which  is  thicker  than  the 
natural  mucous  coat  and  is  much  more  nearly  homogeneous.  The 
disease  is  confined  to  the  mucous  layer.  It  does  not  seem  surprising 
that  a  person  with  the  lining  of  the  stomach  in  such  a  condition 
should  have  vomited  and  been  unable  to  assimilate,  for  there  remains 
hardly  one  of  the  mucous  cells  which  play  so  important  a  part  in 
digestion.  The  vomiting  was  so  obstinate  that  it  was  impossible  to 
decide  during  life  if  the  disease  was  cancer.  The  microscopical  ex- 
amination answered  this  with  an  absolute  negative.  In  another  case 
of  continued  vomiting  combined  with  the  symptoms  of  meningitis  the 
whole  pyloric  end  of  the  stomach  was  found  to  be  four  or  five  times 
thicker  than  natural.  The  thick  portion  was  of  soft  consistence  and 
symmetrical  around  the  pyloric  ring,  instead  of  being  greater  on  one 
side  than  on  the  other,  as  is  usually  the  case  with  cancer,  which  gen- 
erally begins  at  a  single  centre  and  thence  extends.  There  was  great 
thickening  of  the  submucous  and  muscular  coats,  but  no  cells  or  com- 
binations of  cells  characteristic  of  cancer  could  be  found.  It  is  some- 
times easy  to  recognize  cancer  from  the  gross  appearance  of  the  speci- 
men, or,  again,  a  section  examined  with  the  microscope  will  furnish 
the  proof.  In  such  a  case  as  the  one  described,  the  indications  being 
indefinite,  it  is  an  easy  escape  from  a  difficulty  to  say  the  disease  was 
cancer;  but  such  an  assumption  is  neither  scientific  nor  conclusive. 
There  were  symptoms  of  meningitis  during  life,  and  after  death  was 
found  advanced  disease  of  the  peripheral  nerves  within  the  spinal 
canal,  although  none  of  the  cord  itself.  The  result,  therefore,  after 
clinical  study,  post-mortem,  and  microscopical  examination,  was  un- 
certainty as  to  the  cause  of  death.  There  are  few  things  more  puzzling 
than  such  cases  as  the  two  described,  the  first  a  woman  with  lesions 
in  several  organs,  these  being  of  old  age  or  fibroid  nature,  and  the 
second  a  man  with  unrelated  states  of  disease  of  the  nervous  system 
and  stomach.  There  must  be  an  underlying  cause,  which  as  yet  re- 
mains undiscovered,  to  produce  such  strange  results. 


CHAPTER    X. 

THE    INTESTINES. 

WHAT  has  been  said  of  the  stomach  is  true  also  of  the  intestines, — 
that  consistent  study  of  their  gross  and  microscopical  appearances  in 
diseases  not  known  to  produce  lesions  in  them  would  yield  most  use- 
ful information.  Examination  of  the  intestines  is  more  satisfactory  than 
that  of  the  stomach,  for  they  undergo  less  rapid  post-mortem  change. 
Figs.  104  and  105  represent  an  ulcer  of  the  colon  of  a  woman  twenty- 
six  years  old  who  died  of  typhoid  fever.  They  demonstrate  several 
points  of  interest :  first,  ulceration  in  typhoid  fever  does  not  usually 
involve  the  colon,  but  is  confined  to  the  ileum ;  second,  there  are  cavi- 
ties in  the  thickened  submucous  coat ;  and,  third,  there  is  amyloid  dis- 
ease of  the  submucosa.  With  regard  to  the  first,  ulceration  of  the 
colon  in  typhoid  fever,  it  is  interesting,  but  not  extraordinary,  for  in 
any  great  number  of  cases  of  the  disease  ulcers  will  sometimes  be 
found  in  the  large  as  well  as  in  the  small  intestine.  The  cavities  in 
the  tissue  might  possibly  be  taken  to  be  the  result  of  fatty  degenera- 
tion of  the  thickened  submucous  layer,  but  an  examination  of  the 
second  drawing,  made  with  greater  amplification,  shows  that  this  was 
not  the  case.  They  lie  in  the  midst  of  inflammatory  tissue  and  adja- 
cent to  the  region  of  amyloid  deposit,  and  when  thus  seen  consider- 
ably magnified  it  is  evident  from  the  nature  of  their  walls  that  they 
are  not  fat  cells.  One  is  driven  back,  therefore,  to  the  statement 
already  made  in  the  discussion  of  the  cavities  which  are  so  common 
in  the  liver  (page  104),  that  they  cannot  be  explained  as  the  result  of 
fatty  degeneration,  and  that  to  call  them  vacuoles  is  only  to  give  a 
name  to  what  is  not  explained.  There  is  strong  reason  to  suppose 
the  cavities  are  the  effect  of  a  process  akin  to  cystic  degeneration,  if 
they  are  not  simply  cysts  of  small  size.  Whether  fatty  degeneration 
has  any  connection  with  this  disease  cannot  be  now  ascertained.  In 
the  liver  it  was  shown  that  cavities  of  all  sizes,  from  those  which  are 
evidently  the  result  of  fatty  degeneration  to  cysts  large  enough  to  be 
seen  with  the  naked  eye,  may  be  found  in  the  same  liver,  and  it  was 
stated  also  that  in  the  case  of  the  smaller-sized  ones  it  is  impossible 
to  distinguish  precisely  between  fat  cells  and  small  cysts.  The  amy- 
126 


FIG.  104. — ULCER  OF  THE  COLON  SHOWING  AMYLOID  DEPOSIT,     (x  n.) 

From  a  woman  of  twenty-six  years  who  died  of  typhoid  fever,  b  is  placed  over  the  ulcer. 
x,  y,  and  z  are  the  mucous,  submucous,  and  muscular  coats.  The  mucous  coat  is  inter- 
rupted, and  the  submucosa  much  thickened  and  infiltrated  at  the  ulcer.  At  c,  in  the  sub- 
mucosa,  are  many  holes,  and  to  their  right  and  below  them  is  the  amyloid  deposit.  The 
holes  are  such  as  are  commonly  described  as  due  to  fatty  degeneration,  or  as  vacuoles. 
c,  with  the  surrounding  region,  is  represented  more  highly  magnified  by  Fig.  105.  This 
drawing  shows  the  relative  situation  of  the  parts,  but  the  greater  amplification  of  Fig.  105 
is  necessary  for  the  exhibition  of  the  nature  of  the  structural  changes. 

FlG.    105.^-ULCER   OF  THE  COLON   SHOWING   AMYLOID   DEPOSIT.       (X  SO.) 

Enlarged  view  of  the  region  c  of  Fig.  104.  c  indicates  the  holes,  and  below  and 
to  their  right  is  the  amyloid  deposit  (s).  The  deposit  is  in  whorls  or  appears  longitudi- 
nally striated  as  it  happened  to  be  cut,  and  is  infiltrated  with  cells,  as  is  usual  in  amyloid 
material.  At  the  centre  of  the  ulcer  (/•)  is  a  fissure,  and  upon  either  side  of  it  are  areas 
of  round-cell  infiltration.  This  amplification  demonstrates  that  the  holes  are  not  fatty 
deposit.  Fig.  126,  which  represents  typical  amyloid  disease  of  the  kidney,  should  be  ex- 
amined with  this  illustration,  and  it  will  be  seen  how  precisely  alike  the  two  are. 


' 


THE   INTESTINES.  127 

loid  disease  (Figs.  104  and  105)  is  not  of  great  extent,  but  is  very  dis- 
tinct. In  such  a  case,  in  which  the  amount  of  amyloid  deposit  is  small, 
its  relation  to  the  tissue  with  which  it  is  surrounded  can  be  easily 
studied,  and  the  impression  that  the  whole  process  is  only  a  form  of 
fibrosis  becomes  very  strong.  The  amyloid  deposit  has  the  homo- 
geneous and  glassy  look  which  is  characteristic  of  it,  and  through  it 
extend  lines  of  connective  tissue  containing  nuclei.  Such  amyloid 
material  is  exactly  like  some  of  the  forms  of  fibrous  tissue.  The 
difference  is  that  in  most  fibrous  tissues  the  proportion  which  is 
nucleated  is  greater  and  the  structureless  material  less  than  is  seen 
in  Fig.  105.  The  tissue  was  not  subjected  to  the  iodine  test,  for  the 
reason  that  when  the  post-mortem  examination  was  made  there  was 
no  suspicion  of  the  existence  of  amyloid  disease.  The  case  affords 
another  exemplification  of  the  fact  already  so  frequently  dwelt  upon, 
that  in  cases  of  disease  having  definite  pathological  lesions  other 
lesions  quite  foreign  to  those  accepted  as  properly  belonging  to  it  will 
often  be  found  if  sought. 

The  intestines  when  healthy  are  very  thin,  but  they  sometimes 
become  excessively  loaded  with  fat.  The  question  of  the  extent  to 
which  the  organs  may  accumulate  fat  before  it  constitutes  disease  has 
already  been  discussed  (page  8).  The  accumulation  of  a  moderate 
amount  of  fatty  tissue  upon  the  intestines  in  stout  or  elderly  people 
is  not  to  be  looked  upon  as  unhealthy,  but,  on  the  other  hand, 
when  there  is  a  thick  layer  of  fat  upon  their  exterior  and  masses  of 
it  hang  upon  them,  as  is  not  infrequently  seen,  they  must  at  least 
be  sluggish  in  the  performance  of  their  functions,  if  there  is  no  more 
injurious  effect  induced.  In  elderly  people  who  have  died  of  dys- 
entery the  colon  is  so  often  found  thick  and  fatty  that  it  is  likely 
this  is  more  than  coincidence,  nor  is  it  rare  to  find  that  persons 
dead  of  dysentery  had  had  other  chronic  disease,  as,  for  example, 
Bright's  disease  or  chronic  bronchitis.  It  must  not  be  forgotten  that 
the  dysentery  seen  in  this  latitude  is  generally  different  from  the 
dysentery  of  tropical  countries,  which  often  attacks  young  persons  and 
those  who  had  been  previously  in  perfect  health  and  is  rapidly  fatal. 
In  an  elderly  woman  who  died  of  dysentery  and  Bright's  disease 
and  whose  heart  presented  an  extraordinary  development  of  fatty 
infiltration  (see  Figs.  46  and  47)  the  colon  was  in  a  corresponding 
fatty  condition.  When  examined  in  section  it  looked  like  a  piece  of 
adipose  tissue,  and  could  not  have  been  recognized  as  colon  by  its 
appearance  alone.  The  ulceration  had  entirely  removed  the  mucous 


128  THE   ORIGIN   OF   DISEASE. 

follicles,  the  submucous  and  muscular  coats  were  infiltrated  with  fat 
so  as  to  be  beyond  recognition,  and  outside  of  them  was  a  layer  of 
fat  which  was  thicker  than  the  gut  itself.  This  state  of  disease  re- 
sembled in  many  respects  the  fatty  infiltration  of  the  heart  which  was 
found.  In  both  heart  and  colon  the  layer  of  fat  upon  the  outside 
was  thicker  than  the  organs  themselves,  and  the  tissue  was  distorted 
and  split  apart  by  fat-infiltration.  It  is  impossible  not  to  believe  that 
the  deposit  and  infiltration  of  fat  must  have  been  very  destructive  of 
the  power  of  the  organs  to  perform  their  functions.  It  is  probable 
that  the  dysentery  which  was  the  direct  cause  of  death  was  induced 
by  the  fatty  infiltration,  for  tissues  in  process  of  infiltration  with  fat 
are  thrown  into  a  condition  of  exaltation  which  renders  them  liable 
to  inflammation.  A  parallel  can  be  drawn  to  a  certain  extent  be- 
tween very  fat  people  and  fatty  organs.  The  very  fat  are,  as  a  rule, 
puffy  and  incapable  of  as  much  labor  as  those  who  are  better  propor- 
tioned. Their  power  of  sustained  effort  is  reduced,  and  they  are  liable 
to  succumb  to  acute  attacks  so  slight  that  they  could  have  been  easily 
borne  by  persons  of  normal  resisting  power.  The  fat  deposited  in 
and  upon  the  colon  varies  in  character  in  different  cases.  Sometimes 
it  has  the  delicate  and  finely  reticulated  appearance  which  is  character- 
istic of  normal  fat,  and  again  it  may  be  of  much  more  dense  consist- 
ence and  have  bands  of  fibrous  material  running  through  it.  When 
the  latter  is  the  case  it  must  be  considered  that  the  condition  is  partly 
fibroid  disease.  It  will  presently  be  shown  that  this  combination  of 
fibroid  disease  and  adipose  deposit  occurs  in  the  perirenal  fat,  and  it 
has  already  been  discussed  in  connection  with  the  fat  layer  upon  the 
heart.  The  presence  of  small  amounts  of  amyloid  deposit  in  the  in- 
testines, or  at  any  rate  of  material  which  is  so  like  it  that  it  cannot 
be  said  not  to  be  amyloid,  is  very  common.  For  instance,  an  illustra- 
tion has  already  been  given  of  an  arteriole  (Fig.  1 6)  in  the  colon  of 
a  man  who  died  of  dysentery  induced  by  acute  lead  poisoning.  The 
gut  was  enormously  thickened,  the  stage  of  ulceration  not  having 
been  reached,  and  some  parts  of  the  thick  mucous  coat  looked 
amyloid. 

The  study  of  the  pathological  conditions  of  the  intestines  which  I 
have  been  able  to  make  has  not  been  without  profit,  although  less 
satisfactory,  because  less  extensive,  than  that  of  the  heart,  lungs,  liver, 
spleen,  and  kidneys.  The  existence  of  minute  cavities,  probably  the 
result  of  cystic  degeneration,  in  an  ulcerating  colon  indicates  the  likeli- 
hood that  cystic  disease  is  a  common  and  very  generalized  process,  for 


THE   INTESTINES.  129 

it  has  already  been  shown  that  cysts  are  common  in  the  liver  and 
spleen.  If  it  could  be  shown  that  amyloid  disease  is  only  a  form  of 
morbid  fibrosis,  another  link  would  be  formed  in  the  chain  to  connect 
diseases  which  have  been  looked  upon  as  widely  separated,  but  which 
really  are  nearly  related.  It  has  been  taken  for  granted  that  disease 
ordinarily  has  a  single  point  of  origin,  when  in  truth  it  often  arises 
simultaneously  in  several  places,  owing  its  origin  to  causes  as  yet 
beyond  our  comprehension. 


CHAPTER    XL 

THE    KIDNEY. 

THE  pathology  of  the  kidney  has  been  more  thoroughly  and  profit- 
ably studied  than  that  of  any  other  organ,  and  its  anatomy,  to  the 
minutest  details,  is  better  understood.  Its  function  is  one  of  the  most 
important  in  the  economy,  and  a  parallel  may  be  drawn  between  the 
importance  of  the  excretion  of  fluid  from  the  body  and  the  urgent 
necessity  for  its  frequent  imbibition.  Persons  soon  die  of  thirst  if  the 
supply  of  liquid  is  cut  off,  but  starvation  is  a  slow  process.  After  the 
brain,  heart,  and  lung,  the  next  organ  in  importance  is  the  kidney, 
and  its  entire  cessation  to  act  causes  death  more  rapidly  than  any- 
thing except  the  failure  of  one  of  the  three  organs  first  named.  The 
kidney  is  prone  to  disease,  and  it  changes  with  the  progress  of  years 
as  surely  as  wrinkles  come  in  the  faces  of  the  aged.  On  the  other 
hand,  it  is  wonderful  how  tolerant  it  is  of  injury.  Nature  has  made 
such  bountiful  provision  of  renal  tissue  that  a  great  part  of  it  can  be 
diseased  and  yet  a  condition  of  tolerable  health  be  maintained.  It  is 
well  known  that  one  of  the  kidneys  may  be  entirely  destroyed  and 
the  remaining  one  still  suffice  for  the  maintenance  of  life.  The  kid- 
ney in  early  infancy  is  different  in  appearance  and  occupies  a  different 
position  from  the  appearance  it  presents  and  the  position  it  occupies 
in  adults.  In  young  infants  the  capsule  is  thin,  delicate,  and  entirely 
transparent,  and  the  organ  seems  to  stand  out  uncovered  in  the  ab- 
dominal cavity,  although  from  the  anatomical  stand-point  it  is  post- 
peritoneal  and  not  in  the  abdominal  cavity.  The  fat  with  which  it  is 
later  surrounded  is  entirely  wanting.  In  infancy  the  greater  free  cur- 
vature of  the  kidney  projects  much  more  toward  the  front  than  it  does 
in  adult  life,  when  the  organs  are  flat  against  the  back  of  the  body,  the 
hilum  of  each  toward  the  spine,  and  the  greater  curvatures  toward  the 
two  sides.  The  minute  anatomy  of  the  kidney  is  different  in  infants. 
In  preparations  made  for  microscopical  examination,  if  the  plane  of 
section  is  vertical  to  the  surface,  the  tubules  and  vessels  are  cut  in  their 
length,  in  which  case  the  relation  of  the  Malpighian  bodies  to  the 
tubules  is  displayed.  In  such  instances  in  infants  it  can  often  be  seen 
that  the  Malpighian  bodies  are  arranged  around  the  tubules  so  as 
130 


THE   KIDNEY.  131 

to  produce  the  effect  of  a  tree  with  fruit  hanging  from  its  branches. 
There  is  a  central  stem  of  tubules  with  the  rounded  Malpighian  bodies 
disposed  upon  each  side.  This  disposition  of  the  various  parts  is  well 
known  to  histologists,  and  pictures  illustrating  it  are  included  in  many 
works  upon  that  subject.  In  infants'  kidneys  it  is  very  common,  per- 
haps usual,  to  see  this  anatomical  arrangement  more  or  less  well  dis- 
played, but  in  adult  kidneys,  of  which  I  have  examined  ten  times  more 
than  of  infants,  I  have  never  seen  it.  This  experience,  although  not  so 
extensive  as  might  be  desired,  is  sufficient  to  prove  the  point,  that  the 
minute  anatomy  of  the  kidney  changes  as  life  goes  on ;  that  at  later 
periods  confusion  takes  the  place  of  the  beautiful  and  simple  order 
which  existed  when  the  period  of  most  active  development  closed.  As 
a  result  of  disease  this  loss  of  orderly  arrangement  may  be  pushed  to 
its  extreme  limits.  In  the  natural  kidney  large  blood-vessels  exist 
only  at  the  junction  of  the  cortical  and  medullary  portions,  where 
they  enter  the  organ,  for  soon  after  leaving  this  region  they  break  into 
small  twigs,  so  that  the  subcapsular  tissue  contains  no  large  arterioles 
and  but  few  Malpighian  bodies,  which  are  numerous  a  little  deeper  in 
the  organ.  It  will  be  presently  shown  that  in  contracted  kidneys 
large-sized  blood-vessels  are  often  found  close  to  the  external  surface 
beneath  the  capsule,  and  great  numbers  of  Malpighian  bodies  crowded 
nearer  one  another  than  is  natural  in  the  same  region.  This  ex- 
treme distortion  must  be  the  result  of  the  growth  of  the  morbid 
fibroid  tissue,  which  pushes  the  blood-vessels  and  Malpighian  bodies 
toward  the  surface  and  destroys  entirely  the  natural  arrangement.  It 
is  very  common  to  find  cysts  in  the  kidneys  of  old  people,  so  that 
by  many  it  has  been  considered  natural;  but  such  a  conclusion  is 
surely  erroneous,  for  the  formation  of  cysts  in  the  kidneys  is  a  de- 
structive process  as  much  as  is  the  formation  of  cavities  in  the  lungs, 
and  the  one  cannot  be  natural  any  more  than  the  other.  No  one 
would  look  upon  cavities  in  the  lungs  as  a  natural  result  of  old  age. 
To  distinguish  between  the  changes  natural  to  the  advance  of  years 
and  those  of  disease  is  a  difficulty  ever  present  to  the  patholo- 
gist, but  in  the  case  of  cystic  kidneys  it  is  easy  to  decide  to  which 
class  they  belong.  A  singular  antithesis  to  this,  and  at  the  same 
time  a  confirmation  of  its  truth,  is  the  fact  that  the  kidney,  like  all 
the  other  organs,  is  subject  even  in  early  infancy  to  changes  which 
at  later  periods  are  attributed  alternately  to  age  and  to  disease.  At 
six  weeks  I  have  seen  large  thrombi  in  the  renal  veins  and  casts  in 
the  secreting  tubules.  At  five  and  six  months  marasmic  babies — and 


1 32  THE   ORIGIN  OF   DISEASE. 

such  infants  always  resemble  octogenarians — will  often  be  found  to 
have  the  capsules  of  the  kidneys  of  irregular  thickness,  the  fibrous 
tissue  increased,  and  the  tubules  dilated,  just  as  they  ordinarily  are  in 
Bright's  disease.  In  one  of  my  cases,  an  infant  of  six  months,  there 
were  found  several  calcareous  deposits  in  the  kidney  and  a  stone 
which,  after  drying,  weighed  about  one  and  one-fifth  grains  and  was  a 
quarter  of  an  inch  across  in  its  longest  diameter.  The  infant  was  a 
foundling  that  had  been  neglected,  and  it  was  shrivelled  and  wrinkled 
so  that  it  appeared  a  veritable  type  of  age.  This  deposit  of  cal- 
careous matter,  with  the  aged  appearance  of  the  infant,  indicates 
that  tissue-changes  usually  considered  as  natural  to  age  and  those 
of  chronic  disease  are  more  nearly  related  than  at  a  superficial  view 
would  appear.  Since  the  lesions  of  disease  of  such  a  character  are 
to  be  found  in  infancy,  it  is  not  surprising  that  they  exist  also  in 
childhood  and  at  all  later  periods  of  life. 

Fig.  106  represents  a  portion  of  the  kidney  of  a  girl  of  ten  years 
who  died  of  heart  disease  and  who  had  amyloid  degeneration  of  the 
liver,  spleen,  and  kidneys.  There  is  thickening  of  the  capsule,  and 
the  thick  portion  is  sunk  into  the  renal  tissue,  making  a  depression 
beneath  which  the  tissue  is  diseased.  The  Malpighian  bodies  remain, 
but  do  not  appear  healthy,  the  capillary  loops  being  shrunk  and  sur- 
rounded by  a  greater  amount  of  open  space  than  is  natural.  The 
secreting  tubules  have  almost  entirely  disappeared  from  the  diseased 
region,  which  is  in  an  early  stage  of  fibrosis.  In  this  instance  also  the 
thickened  portion  of  the  capsule  is  of  open  structure  and  contains 
many  nuclei,  whereas  in  older  people  and  when  the  disease  is  advanced 
the  fibrous  and  thick  capsule  is  generally  very  solid  and  contains  but 
few  nuclei.  The  disease  as  represented  by  the  drawing  is  typical  of 
the  beginning  of  fibrosis  and  contraction  of  the  kidney,  although  the 
tissue  is  less  solid  than  is  usual  in  older  persons  and  at  more  advanced 
stages.  Fig.  107,  which  is  from  the  same  kidney  as  the  foregoing, 
shows  an  arteriole  passing  into  the  kidney  from  the  perirenal  fat 
through  the  capsule.  It  is  an  anatomical  fact  not  so  generally  known 
as  it  might  be  that,  besides  the  renal  artery  which  enters  at  the  hilum, 
the  kidney  receives  minute  arterial  branches  from  various  sources 
which  pass  directly  through  the  capsule  to  enter  the  substance  of 
the  organ.  When  the  mode  of  development  of  the  kidney  during 
the  embryological  period  is  remembered,  it  seems  as  if  there  must 
have  been  a  time  when  no  vessels  entered  it  through  the  capsule; 
but,  however  this  may  be,  my  experience  has  led  me  to  believe  that 


FIG.  106. — EARLIEST  STAGE  OF  CONTRACTED  KIDNEY,  (x  50.) 

From  a  child  ten  years  old  that  died  of  heart  disease,  e  and  h  indicate  the  boundaries 
of  a  fibroid  area  ;  in  it  the  tubules  have  almost  disappeared,  but  the  Malpighian  bodies 
persist.  In  the  tubules  to  right  and  left  of  the  fibroid  region  the  epithelial  cells  are  ill 
defined.  The  capsule  is  thickened  and  shredded  out,  and  over  the  fibroid  area  it  is  thick- 
est and  dips  downward.  This  thickening  of  the  capsule  with  a  dip  below  the  general  level 
of  the  surface  of  the  kidney  and  an  area  of  fibrosis  under  the  depression  is  characteristic 
of  the  beginning  of  contraction. 

FIG.  107.— ARTERIOLE  ENTERING  THE  KIDNEY  FROM  THE  CAPSULE.     (X  50.) 

Another  area  from  the  same  section  as  Fig.  106.  v  indicates  the  arteriole  which  is 
entering  the  substance  of  the  kidney  from  the  perirenal  fat.  At  the  point  of  entrance 
the  renal  tissue  is  unnaturally  fibroid. 


FIG.  106. 


FIG.  107. 


THE   KIDNEY.  133 

these  capsular  vessels  are  greatly  influenced  by  disease.  It  is  probable 
that  in  fibroid  kidneys  they  increase  in  size  and  prominence  and  in 
numbers.  In  healthy  kidneys  the  vessels  that  penetrate  the  capsule 
are  not  noticeable  in  making  the  ordinary  manipulations  of  a  post- 
mortem examination,  so  minute  are  they,  but  in  contracted  kidneys  if 
the  capsule  is  pulled  off  they  are  seen  to  be  numerous  and  to  appear 
like  stout  cords  binding  the  capsule  to  the  kidney.  The  drawing 
shows  that  at  the  point  of  entrance  of  the  vessel  there  is  disease  of  the 
kidney  of  a  character  similar  to  that  which  has  been  described  in  con- 
nection with  the  preceding  illustration.  There  is  a  slight  pit  of  the 
surface  of  the  kidney  at  the  point  of  entrance,  and  the  capsule  is  thick 
and  the  tissue  in  the  immediate  neighborhood  has  been  condensed  by 
fibrosis,  so  that  in  part  of  it  the  tubules  have  nearly  disappeared,  while 
around  the  fibrous  area  they  are  much  dilated.  In  several  other  in- 
stances I  have  examined  portions  of  diseased  kidneys  containing  one 
of  these  arterioles  passing  through  the  capsule,  and  in  every  one  of 
them  the  point  of  entrance  was  the  seat  of  fibrosis.  This  conjunction 
of  fibrosis  with  vascular  disease  is  very  curious.  It  was  first  described 
by  Gull  and  Sutton  in  their  essays  upon  arterio-capillary  fibrosis  which 
now  belong  to  the  classics  of  medicine.  The  origin  of  the  process  is 
still  unknown,  it  being  impossible  to  decide  whether  it  begins  in  the 
arteries  or  in  the  fibrous  tissue  around  them  or  in  both.  The  child 
from  whose  kidney  the  two  foregoing  illustrations  were  taken  was,  as 
has  been  said,  ten  years  old,  and  it  has  been  made  very  evident  that 
there  was  fibroid  disease.  The  case  illustrated  an  interesting  fact  in 
connection  with  amyloid  degeneration.  The  liver,  spleen,  and  kidneys 
showed  the  peculiar  reaction  of  amyloid  material  when  tested  with 
iodine,  and  the  liver  and  spleen  when  examined  microscopically  were 
seen  to  contain  great  quantities  of  the  deposit.  In  the  kidneys,  how- 
ever, the  evidence  of  amyloid  disease  as  determined  by  the  microscope 
was  so  slight  that  if  it  had  not  been  that  the  liver  and  spleen  were 
so  very  amyloid,  and  that  the  kidneys  had  reacted  to  the  iodine  test, 
it  would  have  been  impossible  to  determine  that  they  were  so  dis- 
eased. The  only  amyloid  deposit  visible  in  the  kidneys  was  in  the 
Malpighian  loops,  in  which  there  were  a  few  of  the  peculiar  homoge- 
neous spots.  The  kidneys  therefore  showed  minute  pittings  of  the 
surface  with  fibroid  tissue  beneath,  and  the  capsule  was  thickened ; 
these  are  the  most  positive  signs  of  contraction  of  an  early  stage ;  but 
besides  all  this  there  were  minute  patches  of  homogeneous  deposit  in 
the  Malpighian  loops  which  were  certainly  amyloid,  for  the  tissue  had 


I34  THE   ORIGIN   OF   DISEASE. 

shown  the  peculiar  reaction  with  iodine,  and  the  liver  and  spleen  were 
in  the  last  stages  of  amyloid  degeneration.  Homogeneous  spots  in 
the  Malpighian  loops,  as  described,  are  in  my  experience  exceedingly 
common  in  chronically  diseased  kidneys,  and  many  times  in  cases  in 
which  they  were  present,  but  in  which  there  was  no  other  reason  to 
suspect  the  existence  of  amyloid  disease,  I  have  been  unable  to  de- 
termine whether  or  not  there  was  amyloid  change.  There  can  be 
no  distinct  line  drawn  separating  fibrosis  from  amyloid  degeneration, 
and,  as  has  been  said  in  connection  with  the  intestines  and  some 
of  the  other  organs,  there  are  many  reasons  for  believing  them  to 
be  only  variations  of  the  same  disease.  At  nine,  twelve,  fourteen,  and 
seventeen  years,  just  as  in  the  case  of  the  girl  of  ten,  I  have  found  in 
the  kidneys  areas  of  fibrosis,  thickening  of  the  capsule,  some  tubules 
greatly  dilated  and  others  very  small,  casts  in  the  tubules,  and  all  the 
other  signs  of  Bright's  disease.  In  children,  therefore,  the  lesions 
of  chronic  disease  of  the  kidney  are  similar  to  those  common  in 
older  persons  and  in  old  age,  and  even  in  infants  of  a  few  months 
the  parallel  holds  good,  for  it  has  been  shown  that  stone  in  the 
kidney,  which  is  usually  a  disease  of  advanced  life,  may  exist  in  an 
infant  of  six  months  with  marasmus. 

Fig.  108  represents  a  minute  fibroid  spot  in  the  kidney  of  a  man  of 
twenty-seven  who  died  of  acute  cholera  morbus  after  an  illness  of  less 
than  forty-eight  hours.  The  existence  of  a  morbid  fibroid  spot  under 
the  circumstances  is  again  illustrative  of  the  fact  so  often  mentioned 
that  lesions  of  chronic  nature  other  than  those  belonging  to  the  dis- 
ease which  caused  death  are  often  found  if  sought.  It  suggests  again 
the  important  question,  To  what  extent  is  the  outcome  of  attacks 
of  acute  disease  influenced  by  the  degree  of  bodily  perfection  of  the 
individual  when  attacked,  and  how  much  more  liable  is  a  person  with 
lesions  of  latent  disease  to  have  acute  attacks  than  one  whose  con- 
dition is  more  nearly  perfect  ? 

The  commonest  disease  of  the  kidneys  is  fibrosis,  or,  as  it  was  for- 
merly more  often  called,  contraction.  Since  the  time  of  Bright  the 
pathological  condition  has  probably  been  more  extensively  investigated 
than  any  other  disease  to  which  man  is  subject.  It  produces  a  great 
variety  of  different  appearances,  both  gross  and  microscopical,  due  to 
the  manner  in  which  the  tissue  is  affected  and  the  extent  to  which  the 
disease  has  progressed. 

Figs.  106  to  115  represent  types  of  fibroid  kidney,  but  they  are 
very  different,  owing  to  the  varying  ways  in  which  the  tissue  has 


FIG.  1 08.—  SMALL  FIBROID  SPOT  IN  THE  KIDNEY,     (x  105.) 

From  a  man  twenty-seven  years  old  who  died  of  acute  cholera  morbus.  a  is  the  fibroid 
area,  which  is  composed  of  connective-tissue  cells  and  fibrous  strands  running  in  many 
directions. 

FIG.  109. — FIBROID  KIDNEY,     (x  15.) 

From  a  man  fifty-seven  years  of  age  who  died  of  Bright' s  disease.  The  capsule  is 
greatly  thickened,  but  especially  so  at  the  middle  part  of  the  picture,  where  it  is  depressed 
below  the  general  level,  and  underneath  it  the  kidney  is  fibroid.  The  tubules  and  epi- 
thelium have  here  disappeared,  and  their  place  is  taken  by  fibrous  tissue  and  the  round 
cells  of  inflammatory  tissue.  This  fibre-inflammatory  material  is  most  dense  and  in  greatest 
mass  directly  beneath  the  thickest  and  depressed  portion  of  the  capsule,  and  from  this  it 
branches  out  in  various  directions.  The  tubules  which  occupy  the  space  between  the 
fibroid  lines  and  patches  are  almost  all  dilated  so  as  to  be  much  larger  than  natural.  Mal- 
pighian  bodies  in  various  stages  of  destruction  are  scattered  through  the  tissue. 


i<;.  108. 


Kit;.  109. 


THE   KIDNEY.  135 

been  destroyed.  It  is  not  easy  to  be  certain  which  manner  of  de- 
struction is  the  most  common,  but  probably  it  is  that  represented  by 
Fig.  109,  which  is  from  the  kidney  of  a  man  of  fifty-seven  who  died 
of  Bright's  disease  with  extensive  fibrosis  of  most  of  the  organs  and 
deposits  of  chalk  in  a  great  many  different  tissues.  The  capsule  is 
greatly  thickened,  and  where  thickest  is  sunk  into  the  kidney  tissue, 
making  a  depression  below  the  general  surface  level.  Beneath  this 
depression  is  a  fibroid  area  which  examination  under  greater  ampli- 
fication would  show  to  be  composed  of  round-cell  infiltration  and 
fibrous  strands,  interspersed  with  Malpighian  bodies  in  various  stages 
of  fibroid  destruction.  Epithelium  and  all  appearance  of  tubules 
have  almost  entirely  disappeared  from  the  fibroid  areas.  Scattered 
all  through  the  tissue  are  fibrous  strands  similar  to  the  large  mass 
beneath  the  thickened  and  depressed  portion  of  the  capsule,  and 
it  appears  as  if  these  strands  had  grown  by  extension  from  the  main 
fibroid  mass.  The  remaining  renal  tissue  is  still  composed  of  epithe- 
lium, but  almost  all  the  tubules  are  dilated  so  that  they  are  very  much 
larger  than  natural.  It  is  striking  how  the  disease  seems  to  have  its 
centre  and  to  have  originated  at  the  external  surface  of  the  kidney  in 
a  region  where  the  capsule  is  thickened  and  depressed  and  the  tissue 
beneath  fibroid.  Such  lesions  look  like  a  further  development  of 
what  has  already  been  illustrated  by  Fig.  106  as  the  earliest  stage 
of  contracted  kidney.  In  this  form  of  fibrosis  the  greatest  portion  of 
the  tissue  is  natural,  consisting  of  tubules  lined  with  epithelium.  The 
tubules,  although  very  much  dilated,  were  not  so  greatly  injured  but 
that  they  could  perform  their  function  and  in  case  of  the  recovery  of 
the  patient  might  have  again  become  natural.  The  clinical  history  of 
such  cases  usually  is  that  the  excretion  of  urine  had  been  sufficiently 
good  for  the  maintenance  of  life,  and  that  the  direct  cause  of  death 
was  to  be  sought  elsewhere  than  in  the  kidney,  probably  in  the  lungs 
or  the  heart,  although  according  to  the  accepted  method  of  classifica- 
tion of  the  day  the  case  was  called  Bright's  disease  of  the  kidney. 

Fig.  no  represents  a  portion  of  kidney  from  a  man  fifty-one  years 
old  who  died  of  perihepatic  abscess.  The  diagnosis  during  life  was 
typhoid  fever,  and,  although  the  symptoms  were  not  typical  and  the 
diagnosis  was  not  considered  satisfactory  or  conclusive,  a  more  accu- 
rate one  could  not  have  been  made.  It  was  only  at  the  post-mortem 
examination  that  a  large  perihepatic  abscess  was  found  to  be  present 
and  no  lesions  of  typhoid  fever  whatever.  The  drawing  includes  a 
portion  of  the  kidney  with  the  capsule  and  some  perirenal  fat.  The 


136  THE   ORIGIN   OF   DISEASE. 

condition  is  different  from  that  last  described.  Instead  of  the  disease 
being  scattered  in  spots,  the  whole  of  the  tissue  is  diseased.  The 
effect  produced  is  that  of  a  fine  fibrous  tissue  with  Malpighian  bodies 
and  epithelial  tubules  scattered  through  it.  The  amount  of  epithelium 
is  insignificant  and  that  of  fibrous  tissue  enormous,  and  it  has  forced 
the  tubules  apart  so  that  hardly  any  two  are  in  contact  as  is  natural. 
The  tubules  are  all  narrowed  and  some  nearly  closed,  a  condition  very 
different  from  that  shown  in  Fig.  109,  in  which  the  tubules  are  dilated. 
The  Malpighian  bodies  are  in  all  stages  of  fibroid  destruction.  The 
capsule  is  thick  and  of  coarser  texture  than  natural,  and  the  fibrous 
strands  composing  it  do  not  all  run  parallel  with  one  another  to  pro- 
duce a  smooth  outer  surface,  but  many  of  the  surface  strands  run  off 
at  right  angles  to  the  general  line  of  the  capsule.  These  right-angled 
fibrous  bands  run  out  into  the  perirenal  fat  and  are  sometimes  con- 
tinuous with  fibrous  tissue,  of  which  there  are  strings  running  in 
various  directions  through  the  fat.  This  condition  of  fibrosis  of  the 
perirenal  fat  with  thickening  of  the  kidney  capsule  and  close  binding 
together  of  the  capsule  and  fat  is  a  very  common  accompaniment  of 
contraction  of  the  kidneys,  and  it  has  been  shown  that  a  parallel  con- 
dition occurs  in  the  heart  and  its  fatty  layer.  A  portion  of  the  same 
section  is  represented  more  highly  magnified  by  Fig.  in  (see  descrip- 
tion), which  shows  one  Malpighian  body  very  fibroid,  others  some- 
what shrunken,  the  tubules  undergoing  atrophy,  and  that  much  the 
larger  part  of  the  kidney  included  in  the  drawing,  instead  of  being 
almost  entirely  epithelium,  as  would  be  natural,  is  composed  of  fibrous 
tissue.  Details  of  structure  are  better  shown  by  this  drawing,  but  the 
general  effect  of  the  universal  growth  of  fibrous  tissue,  the  thickening 
of  the  capsule,  and  the  unnatural  adhesion  to  it  of  the  perirenal  fat, 
which  is  also  unnaturally  fibrous,  all  characteristic  features  of  the  form 
of  contraction,  are  seen  at  a  glance  in  the  low-power  picture. 

Fig.  112  illustrates  a  third  form  of  fibrosis.  It  is  a  portion  of  the 
kidney  of  a  man  of  fifty-eight  who  died  of  Bright's  disease.  This 
kidney  is  strikingly  like  inflamed  emphysematous  lung,  which  when 
examined  under  moderate  amplification  appears  as  a  solid  tissue  with 
open  spaces  scattered  through  it,  the  solid  portion  being  lung  tissue 
of  which  the  alveoli  have  been  filled  with  exudate,  and  the  open 
spaces  dilated  and  broken  air-sacs  which  have  remained  empty.  The 
kidney  is  diseased  so  that  it  is  almost  beyond  recognition.  Only  a 
small  portion  of  the  tissue  included  in  the  drawing  is  composed  of 
the  epithelial  tubules,  most  of  it  being  fibrous  material  which  is  rich 


FIG.  no. — FIBROID  KIDNEY,     (x  16.) 

From  a  man  fifty-one  years  old  who  died  of  perihepatic  abscess.  This  presents  a 
strong  contrast  with  Figs.  109  and  112.  The  disease  is  generalized  instead  of  being  in 
spots  ;  everywhere  there  is  a  great  increase  of  fibrous  tissue,  which  is  translucent  and 
poor  in  cells,  the  Malpighian  bodies  are  small,  the  tubules  of  small  calibre,  and  the  total 
amount  of  epithelial  tissue  reduced  so  greatly  as  to  be  insignificant.  The  capsule  is 
thickened,  and  there  extend  from  it  fibrous  strands  which  ramify  in  the  perirenal  fat. 
The  area  indicated  by  u  is  represented  in  Fig.  in  more  highly  magnified. 

FIG.  in.— FIBROID  KIDNEY,     (x  50.) 

The  area  u  in  Fig.  1 10,  more  highly  magnified.  This  shows  the  nature  of  the  fibrous 
tissue, — that  it  is  poor  in  cells,  and  that  the  amount  of  epithelial  tissue  is  diminished  and 
its  cells  are  disintegrated,  q  is  a  fibroid  Malpighian  body. 


FIG.  no. 


FIG.  in. 


FIG.  112. — FIBROID  KIDNEY  (RESEMBLING  PULMONARY  EMPHYSEMA),     (x  10.) 

From  a  man  of  fifty-eight  years  who  died  of  Bright's  disease.  The  general  appearance 
recalls  that  of  pulmonary  emphysema  ;  the  patches  containing  dilated,  broken  tubules  which 
are  adjacent  to  the  surface  and  project  beyond  the  general  level  are  like  emphysematous 
blebs  on  the  surface  of  lung ;  there  is  great  increase  of  fibrous  tissue,  which  is  very  dense 
and  rich  in  inflammation  cells  ;  the  epithelial  elements  which  remain  present  themselves 
as  islands  in  a  sea  of  diseased  fibrous  tissue.  These  epithelial  islands  consist  of  dilated 
tubules  and  tubules  with  broken  walls,  like  lung  alveoli  in  emphysema.  The  contrast  of 
this  mode  of  destruction  with  that  depicted  in  Figs.  109  and  no  is  most  striking,  g  is 
placed  above  the  area  represented  more  highly  magnified  in  Fig.  113. 

FIG.  113. — FIBROID  KIDNEY  (RESEMBLING  PULMONARY  EMPHYSEMA),     (x  50.) 

Enlarged  view  of  the  area  g  in  Fig.  112.  The  capsule,  which  is  greatly  thickened,  is 
raised  over  the  central  region  which  contains  the  dilated  and  broken  tubules,  and  dips 
slightly  over  the  fibroid  areas  to  right  and  left.  A  Malpighian  body  is  included  in  the 
central  region.  The  great  density  of  the  fibrous  tissue  and  its  richness  in  the  round  cells 
of  inflammation  are  well  represented.  In  what  respect  does  this  process  of  destruction 
differ  from  that  of  emphysema  of  the  lung  ? 


FlO.    112. 


THE   KIDNEY.  137 

in  inflammation-cells.  There  are  areas  containing  dilated  tubules 
whose  walls  have  broken  so  that  they  form  good-sized  open  spaces 
scattered  through  the  general  fibroid  mass.  Several  of  these  open 
patches  are  at  the  surface,  and  in  such  instances  they  form  projections 
so  closely  resembling  emphysematous  blebs  upon  the  surface  of  the 
lung  as  to  suggest  a  parallelism  of  the  two  states  of  disease.  There 
is  always  fibrosis  with  emphysema  of  the  lungs,  and  its  most  salient 
feature  is  the  way  in  which  the  walls  of  the  air-sacs  break  down  to 
form  large  empty  spaces  exactly  as  has  happened  to  these  renal 
tubules.  The  drawing  includes  the  entire  depth  of  the  kidney  from 
the  capsule  to  the  hilum,  and  therefore  shows  all  the  parts.  The 
differentiation  of  the  medullary  from  the  cortical  substance,  which  in 
healthy  kidney  is  very  sharp,  has  been  entirely  destroyed  by  the  dis- 
ease, so  that  straight  tubules,  labyrinths,  cortex,  and  medulla  are  all 
alike,  except  that  the  largest  vessels  are  confined  to  the  region  of  the 
hilum.  The  appearance  of  the  kidney  affords  a  most  striking  confir- 
mation of  the  statement  that  disease  often  entirely  destroys  natural 
topographical  arrangements.  One  of  the  large  arteries  is  filled  with  a 
thrombus,  and  when  the  section  is  examined  with  sufficient  amplifi- 
cation it  is  seen  that  all  the  arteries  are  greatly  thickened  and  dis- 
eased. The  most  common  condition  of  these  arteries  is  thick  walls, 
tending  to  close  the  calibres.  The  tissue  forming  the  walls  is  much 
more  homogeneous  than  natural  and  is  poor  in  cells ;  therefore  the 
differentiation  of  the  coats  is  nearly  lost.  Such  arterioles  strongly 
resemble  vessels  which  have  undergone  the  amyloid  change.  Most 
of  the  Malpighian  bodies  are  fibroid,  they  are  generally  reduced  in 
size,  and,  like  the  walls  of  the  arterioles,  tend  to  be  homogeneous. 
In  some  instances  it  is  difficult  to  distinguish  between  arterioles  and 
Malpighian  bodies,  to  such  a  degree  has  the  fibroid  degeneration 
changed  them,  and  yet  few  things  are  more  unlike  than  healthy  Mal- 
pighian bodies  and  arterioles.  Fig.  1 1 3  represents  a  small  portion  of 
the  tissue  shown  by  Fig.  112,  but  more  highly  magnified.  It  makes 
even  more  evident  the  resemblance  to  an  emphysematous  bleb  upon 
the  surface  of  the  lung.  The  central  region  contains  enormously 
dilated  tubules  with  broken  walls,  so  that  large  cavities  are  formed. 
The  epithelium  is  degenerated,  and  there  is  fibrous  tissue  scattered 
among  the  tubules.  A  Malpighian  body  with  dilated  capsule  whose 
capillary  loop  is  undergoing  atrophy  is  included.  The  central  region 
is  entirely  surrounded  by  fibrous  tissue,  and  over  it  is  the  capsule  of 
the  kidney,  which  is  thickened  and  raised  above  the  general  level, 


138  THE   ORIGIN   OF   DISEASE. 

while  to  right  and  left  over  the  fibrous  areas  it  is  drawn  downward  by 
the  contraction  which  is  so  common  in  fibrous  tissue.  The  fibrous 
tissue  is  more  dense  than  usual  in  the  kidney,  and  hardly  any  trace  of 
the  normal  elements  composing  kidney  can  be  seen  in  it.  It  is  likely 
that  a  kidney  such  as  this  was  very  unfit  to  perform  its  function,  if 
it  was  not  entirely  useless.  Substituting  liquid  contents  for  air,  the 
parallelism  of  the  appearance  of  this  fibroid  destruction  of  the  kidney 
with  that  of  pulmonary  emphysema  is  so  close  that  it  can  hardly  be 
exaggerated.  The  parallelism  also  extends  to  the  manner  in  which 
the  two  forms  of  disease  have  their  origin. 

Fig.  1 14  represents  a  transverse  section  across  the  entire  kidney  of 
a  man  of  thirty-one  who  died  of  Bright's  disease.  It  is  an  instance 
of  extreme  contraction  of  the  kidney,  being  three-quarters  of  an  inch 
across  in  the  long  and  one-quarter  in  the  short  diameter.  Of  course 
it  was  not  so  small  as  this  when  removed  from  the  body,  as  there 
is  always  some  shrinkage  in  preparing  tissue  for  section.  The  other 
kidney  was  much  larger,  but  it  also  was  extremely  fibroid.  It  is 
difficult  to  imagine  anything  that  would  show  better  than  this  kidney 
does  distortion  of  natural  relations ;  there  is  no  distinction  into  cortex 
and  medulla,  but  a  confused  collection  of  fibrous  tissue,  fat,  blood- 
vessels, and  diseased  renal  tissue.  The  blood-vessels  even  with  this 
low  amplification  can  be  seen  to  be  greatly  thickened,  some  of  them 
almost  closed.  When  more  magnified  they  show  a  great  variety  of 
arterial  disease,  which  is  generally  the  case  in  fibroid  and  contracted 
kidney.  The  number  of  vessels  in  proportion  to  the  area  of  tissue  is 
very  great,  recalling  to  some  extent  the  appearance  of  an  angioma, 
but  it  must  be  remembered  that  this  is  a  directly  opposite  condition, 
a  retrogression,  the  result  of  shrinking  instead  of  growth  and  increase, 
such  as  take  place  in  an  angioma.  The  increased  proportional  num- 
ber of  vessels  is  due  to  the  fact  that  they  are  of  such  structure  as  to 
be  difficult  to  destroy,  and,  while  much  of  the  renal  secreting  sub- 
stance disappears  in  the  course  of  contraction,  the  vessels,  on  the  con- 
trary, persist  in  very  great  numbers  and  are  diseased  and  thickened. 
Such  thickened  and  diseased  vessels  can  under  no  circumstances  be 
studied  to  greater  advantage  than  in  contracted  kidneys,  in  which  they 
are  found  presenting  every  kind  of  histological  growth  and  destruc- 
tion, and  an  infinite  variety  of  changes  of  the  relations  and  appearance 
of  the  three  coats.  Arteries  are  much  more  persistent  in  contracted 
kidneys  than  veins,  and  a  great  many  more  of  them  remain,  or  else 
this  effect  is  produced  by  the  fact  that  the  veins  have  become  so 


FIG.  114. — CONTRACTED  KIDNEY.     (X  6.) 

A  transverse  section  across  the  entire  kidney  of  a  man  of  thirty-one  years  who  died 
of  Bright' s  disease.  The  capsule  is  greatly  and  irregularly  thickened,  and  fibrous  strands 
extend  from  it  into  the  perirenal  fat ;  it  contains  a  good  many  blood-vessels.  The  fibroid 
Malpighian  bodies  and  round-cell  infiltration  cannot  be  clearly  distinguished  with  such 
low  amplification.  The  arteries  are  very  numerous  and  their  walls  greatly  thickened. 
Quite  large  arteries  are  seen  in  the  renal  tissue  itself,  w  is  a  portion  of  a  calyx  connected 
with  the  ureter.  The  proportion  of  fat  to  renal  tissue  is  very  large. 


1mm 


FIG.  115.— CONTRACTED  KIDNEY.     (X  4-) 

Section  across  the  kidney  of  a  woman  forty-two  years  of  age  who  died  of  cerebral 
apoplexy.  The  direction  of  section  is  dorso-ventral,  exhibiting  the  horseshoe  shape.  #., 
a,  a  are  arteries,  which  are  very  numerous  and  some  of  them  quite  close  to  the  capsular 
surface.  Even  with  the  low  amplification  it  is  seen  that  they  are  thick-walled,  v,  a  vein 
containing  clotted  blood.  c,  Malpighian  bodies,  of  which  there  are  many  close  to  the 
surface.  They  are  almost  all  fibroid,  but  this  can  be  distinctly  seen  only  with  greater  am- 
plification, h,  the  hilum,  containing  much  fat,  but  made  to  appear  larger  than  it  was  during 
life,  for  the  two  halves  of  the  kidney  spread  apart  somewhat  in  process  of  preparation. 
The  hilum  contains  fat,  blood-vessels,  etc.,  and,  although  its  size  is  exaggerated,  it  was  quite 
large  before  the  spreading  of  the  two  halves  of  the  kidney  occurred,  and  thus  the  organ 
appeared  larger  than  it  really  was.  d  is  an  exceedingly  narrow  region.  A  noticeable 
feature  is  the  irregular  distribution  of  the  contraction,  the  amount  of  tissue  upon  one  side 
of  the  hilum  being  nearly  twice  as  great  as  upon  the  other. 


FIG.  115. 


THE   KIDNEY.  139 

thickened  by  disease  that  they  can  no  longer  be  distinguished  from 
arteries.  It  is  inconceivable  that  all  the  blood-vessels  which  existed 
in  this  kidney  when  it  was  of  the  full  natural  size  are  still  present 
in  the  reduced  organ  which  survived  the  disease,  and  it  is  therefore 
almost  certain  that  the  vessels  which  were  destroyed  contributed  their 
part  toward  the  formation  of  the  fibrous  tissue  by  having  their  open- 
ings entirely  occluded  and  thus  becoming  solid  cords.  This  belief  is 
warranted  by  the  fact  that  the  whole  tendency  of  the  vessels  is  toward 
increase  of  their  fibrous  tissue,  thickening,  and  finally  entire  closure, 
for  it  is  not  rare  to  see  a  vessel  with  its  lumen  entirely  obliterated. 
The  most  striking  feature  of  all,  perhaps,  shown  by  the  drawing  in 
connection  with  the  blood-vessels  is  their  displacement  from  their 
natural  position.  In  natural  kidney  the  vessels  enter  its  substance  at 
the  junction  of  the  cortical  and  medullary  portions  and  quickly  break 
up  into  small  twigs,  so  that  no  large  ones  exist  in  the  cortical  sub- 
stance near  the  surface.  In  this  organ,  owing  to  the  distortion  and 
dragging  effect  of  the  growing  fibrous  tissue,  large  vessels  are  seen 
in  the  secreting  substance,  and  good-sized  ones  have  been  pushed 
so  far  from  their  natural  position  as  to  lie  near  the  capsule.  The 
portions  of  perirenal  fat  included  contain  many  blood-vessels,  a  few 
of  which  are  shown  by  the  drawing.  When  it  is  studied  with  greater 
amplification  it  can  be  seen  to  contain  many  new  blood-vessels  of  the 
kind  that  grow  in  tissues  developed  as  the  result  of  disease.  Besides 
the  evidence  of  a  morbid  condition  afforded  by  the  presence  of  these 
new  blood-vessels,  the  perirenal  fat  is  more  fibrous  than  natural,  and, 
what  is  especially  notable,  there  are  fibrous  strands  extending  from 
the  thickened  and  coarse  capsule  into  the  fat  and  firmly  binding  cap- 
sule and  fat  together,  as  is  usual  under  the  circumstances.  Another 
feature  exhibited  by  the  drawing — and  it  is  one  which  should  always 
be  considered  in  estimating  the  size  of  a  contracted  kidney — is  that 
there  is  a  great  deal  of  fat  in  the  hilum  and  about  the  ureter  and 
calyces.  This  is  a  very  common  occurrence ;  and  it  is  often  the  case 
that  when  there  is  but  little  secreting  substance  the  organ  is  made  to 
appear  much  larger  than  it  really  is  by  the  stuffing  of  the  hilum  with 
fat.  The  Malpighian  bodies  are  in  all  stages  of  fibroid  degeneration, 
but  it  requires  greater  amplification  to  show  this.  The  other  kidney 
was  cystic. 

Fig.  115  represents  a  section  across  the  entire  kidney  of  a  woman 
of  forty-two  who  died  of  cerebral  apoplexy.  It  is  about  one  inch 
across  in  each  of  its  diameters,  and  therefore  was  extremely  con- 


i4o  THE   ORIGIN   OF   DISEASE. 

tracted.  This  kidney  shows  a  condition  in  many  respects  similar  to 
that  of  the  last  described,  but  it  demonstrates  irregularity  of  distri- 
bution of  the  contraction,  the  Malpighian  bodies  and  blood-vessels 
having  been  pushed  to  the  surface,  and  the  organ  appearing  larger 
than  it  really  was,  owing  to  the  filling  of  the  hilum  with  fat.  With 
regard  to  the  irregularity  of  the  contraction,  a  glance  shows  that  the 
portion  of  kidney  upon  one  side  of  the  hilum  is  nearly  twice  as  large 
as  upon  the  other,  and,  further,  that  at  the  point  opposite  the  opening 
of  the  hilum  the  secreting  substance  is  reduced  to  such  an  extent  that 
only  a  narrow  bridge  remains  to  join  the  two  halves  of  the  kidney 
together.  Near  this  narrow  part  and  elsewhere  toward  the  capsular 
surface  the  blood-vessels  and  fibroid  Malpighian  bodies  can  be  seen 
in  great  numbers  lying  so  near  as  almost  to  touch  the  capsule.  Into 
this  position  they  were  forced  by  the  growth  of  fibrous  tissue  and 
shrinking  of  the  organ,  for,  as  has  been  said,  in  natural  kidney  large 
blood-vessels  are  to  be  found  only  at  the  junction  of  the  cortex  and 
medulla,  and  in  the  region  directly  adjacent  to  the  capsule  there  are 
but  few  Malpighian  bodies.  The  drawing  shows  distinctly  that  there 
was  more  fat  than  natural  in  the  hilum,  but  at  the  same  time  it  exag- 
gerates this  condition  somewhat,  for  in  course  of  preparation  the  two 
halves  of  the  kidney  were  forced  farther  apart  than  they  were  during 
life.  Such  low  amplification  was  used  in  making  the  picture  that  many 
details  of  structure  fail  to  show  which  are  easily  distinguished  when 
it  is  more  highly  magnified,  as  for  instance  in  the  portions  rendered 
by  long  flowing  lines. 

Fig.  1 1 6  is  from  the  kidney  of  a  man  of  seventy  who  died  of  chronic 
myelitis  and  who  had  very  contracted  kidneys.  It  is  to  show  a  tubule 
exceedingly  narrowed  and  deformed  which  lies  isolated  in  the  midst 
of  fibrous  tissue.  The  condition  is  parallel  with  what  has  been  shown 
to  occur  in  the  liver  in  hypertrophic  cirrhosis,  under  which  circum- 
stances a  column  of  hepatic  secreting  cells  may  be  compressed  to  such 
an  extent  as  to  look  like  a  secreting  tubule  in  the  early  stage  of  its 
embryological  development.  The  reasons  for  believing  this  disease 
of  the  liver  to  be  a  retrogression  owing  to  atrophy  of  the  columns 
of  secreting  cells,  and  not  a  development  of  new  bile-ducts  as  has 
been  commonly  supposed,  have  already  been  discussed.  The  kidney 
tubule  is  surrounded  by  fibrous  tissue,  no  others  being  adjacent  to 
it  as  in  healthy  kidney.  At  one  end  of  it  the  epithelial  cells  have 
disappeared,  and  it  appears  to  be  composed  of  fibrous  substance, 
while  at  the  other  the  epithelial  cells  are  squeezed  together  so  that 


FIG.  116. — RENAL  TUBULE  COMPRESSED  BY  FIBROSIS.     (x  220.) 

From  a  man  of  seventy  years  who  died  of  chronic  myelitis,  b  is  a  large  secreting 
tubule  ;  c,  a  capillary ;  d,  the  compressed  narrow  tubule.  It  lies  embedded  in  fibrous 
tissue,  and  its  cells  are  flattened  from  pressure.  The  contrast  in  size  between  d  and  b 
is  striking.  As  the  region  shown  is  close  to  the  capsule,  it  cannot  be  that  the  narrow 
tubule  is  one  of  the  loops  of  Henle,  which  are  naturally  very  small.  The  destruction 
by  pressure  here  depicted  resembles  that  shown  in  the  liver  by  Fig.  83. 

FIG.  117. — CALCAREOUS  DEPOSIT  IN  THE  KIDNEY,     (x  105.) 

From  a  man  seventy  years  of  age  who  died  of  chronic  myelitis  and  who  had  con- 
tracted kidneys.  The  section  was  cut  from  the  medullary  region  across  one  of  the  papillae 
near  its  apex,  and  therefore  includes  the  largest-sized  tubules,  a  is  an  arteriole,  while  all 
the  other  large  openings  are  tubules,  c  is  calcareous  deposit  which  is  seen  to  lie  in  the 
tissue  around  most  of  the  tubules  and  even  in  the  wall  of  the  arteriole  (a).  The  kidney 
was  exceedingly  fibroid,  and  so  changed  by  disease  that  none  of  the  epithelial  lining  of  the 
tubules  remains.  There  was  no  calcareous  material  within  the  calibres  of  the  tubules. 
The  deposit  of  mineral  matter  in  the  tissue  around  a  cyst  in  the  liver  is  shown  by  Fig.  80. 


FIG.  1 1 6. 


THE   KIDNEY.  141 

they  lie  in  contact  and  the  lumen  of  the  tube  is  closed.  The  cells 
are  so  distorted  that  they  are  oval  and  their  greatest  diameter  is 
parallel  with  the  length  of  the  tube.  These  cells  are  exactly  like 
those  which  sometimes  form  the  wails  of  cysts,  as,  for  instance,  in  the 
spleen  and  kidneys  (Figs.  97  and  123).  This  narrow  renal  tubule 
which  was  in  process  of  atrophy  is  interesting,  both  because  it  shows 
one  method  of  destruction  of  the  secreting  substance  of  the  kidney 
during  contraction,  and  because,  owing  to  its  striking  resemblance  to 
the  atrophying  cells  of  the  liver  (Fig.  83),  it  lends  confirmatory  evi- 
dence to  the  view  that  such  things  as  these  narrow  shrunken  columns 
of  cells  in  the  liver  and  kidneys  are  only  parts  of  the  great  generalized 
process  of  fibrosis  which  goes  on  with  the  advance  of  years  or  in  the 
young  as  a  result  of  disease. 

Fig.  117  is  from  the  same  section  as  the  preceding.  The  purpose 
of  the  drawing  is  to  show  the  early  stage  of  the  deposit  of  mineral 
matter  in  the  kidney.  This  is  of  very  frequent  occurrence  in  con- 
tracted kidneys,  and,  as  illustrations  of  the  appearances  are  not  in- 
cluded in  any  text-book  of  pathology  with  which  I  am  acquainted, 
it  seemed  worth  while  to  make  a  demonstration  of  the  phenomenon. 
The  drawing  is  of  a  section  across  one  of  the  cones  not  far  from  its 
papilla,  and  it  shows  tissue  so  changed  by  the  fibroid  process  that  all 
trace  of  epithelial  lining  of  the  tubes  has  disappeared  and  the  tubules 
appear  as  empty  rings  of  fibroid  tissue.  The  salt  deposit  lies  in  the 
tissue  around  the  tubules  and  even  in  the  wall  of  an  arteriole  (see 
description  of  plate),  and  it  has  had  a  tendency  to  dispose  itself  in 
rings  around  the  openings  rather  than  to  be  scattered  loosely  in  dis- 
ordered masses  in  the  tissue.  There  is  no  mineral  matter  lying 
within  the  calibres  of  any  of  the  tubules.  For  my  own  part,  I  have 
never  seen  mineral  matter  within  the  tubules  after  death,  although  it 
is  so  common  an  occurrence  for  patients  to  pass  sand  and  concretions 
in  the  urine.  Deposits  such  as  those  so  well  shown  by  the  drawing 
are  quite  common  in  the  kidney,  and  the  deposit  of  mineral  matter  in 
the  tissue  around  a  small  cyst  in  the  liver  has  already  been  described 
(Fig.  80).  Parrot  *  speaks  of  the  deposit  of  urate  of  sodium  in  the 
collecting  tubules  of  the  medullary  portion  of  the  kidney  as  being  a 
common  occurrence  in  foundlings  dead  of  marasmus.  This  I  have 
never  been  able  to  find  in  any  of  the  young  infants  that  I  have  ex- 
amined, although  I  have  found  deposits  in  the  renal  substance  like 
those  shown  by  the  drawing,  and  mention  has  already  been  made  of 

*Clinique  des  Nouveau-N6s,  L'Athrepsie,  par  J.  Parrot,  Paris,  1877. 


142  THE   ORIGIN   OF   DISEASE. 

a  stone  found  in  the  kidney  of  an  infant  of  six  months.  In  the  case 
of  a  stone  of  such  size  it  would  be  impossible  to  ascertain  where  it 
originated,  for  in  the  course  of  its  growth  it  would  force  itself  into 
surrounding  parts  and  break  through  the  substance  in  which  it  lay  at 
the  time  of  its  beginning. 

Fig.  118  represents  a  portion  of  the  kidney  of  a  man  thirty-two 
years  of  age  who  died  of  Bright's  disease  and  heart  disease.  It  is  a 
type  of  one  form  of  contracted  kidney ;  there  is  fibrosis  of  the  medul- 
lary portion  to  a  greater  degree  than  usual,  and  there  is  a  small  spot 
which  is  in  many  respects  like  a  malignant  new  growth.  The  discus- 
sion of  this  latter  feature  will  be  taken  up  later.  The  general  type 
of  the  fibrosis  of  the  cortical  portion  is  the  same  as  that  shown  by 
Fig.  109,  and  its  peculiarities  need  not  be  repeated.  So  far  as  con- 
cerns the  medullary  portion  of  the  kidney  it  is  hardly  necessary  to 
say  that  in  cases  of  contracted  kidney  it  bears  its  share  in  the  process 
of  disease,  and  becomes  fibroid  at  the  same  time  with  the  cortex. 
Extreme  fibrosis  of  the  medulla  is  shown  by  the  illustration  last 
described,  and,  as  already  stated,  it  was  from  the  greatly  contracted 
kidney  of  a  man  seventy  years  old.  Besides  the  mineral  matter  in 
the  tissue  around  the  tubules  and  arteriole,  which  is  its  most  pecu- 
liar characteristic,  the  changed  condition  of  the  whole  of  the  renal 
tissue  is  striking.  Natural  kidney  consists  in  largest  part  of  epithelial 
elements,  and  through  it  there  is  a  small  amount  of  fibrous  material 
which  carries  the  numerous  blood-vessels  and  affords  a  supporting 
framework  for  the  tubules ;  but  in  this  instance  no  epithelium  is  to 
be  seen,  and  most  of  it  is  fibrous  tissue  poor  in  nuclei.  This  is  no 
more,  perhaps,  than  might  be  expected  when  it  is  recalled  that  it 
was  the  case  of  an  old  man  with  a  kidney  greatly  reduced  in  size  and 
excessively  fibroid.  The  medullary  portion  simply  partook  in  the 
general  process  of  disease,  and  its  epithelium  atrophied  and  disap- 
peared and  fibroid  tissue  replaced  it  at  the  same  time  with  the  fibroid 
destruction  of  the  cortex.  Fig.  1 18  is  an  instance  of  fibrosis  of  another 
kind,  for  the  patient  was  a  man  in  middle  life  who  died  of  a  compara- 
tively acute  attack,  and  whose  kidney,  although  contracted  and  fibroid, 
shows  the  disease  under  a  very  different  aspect.  The  drawing  shows 
that  the  medullary  portion  is  fibroid,  the  amount  of  epithelium  being 
much  less  than  normal  and  that  of  fibrous  tissue  increased,  but,  as 
this  also  was  an  instance  of  contracted  kidney  with  unmistakable 
disease  of  the  cortex,  it  is  not  surprising  that  the  medulla  as  well  as 
the  cortical  portion  should  have  been  diseased.  The  way  in  which 


FIG.  118. — GENERAL  RENAL  FIBROSIS,  FIBROSIS  OF  THE  MEDULLARY  PORTION,  AND 
A  GROWTH  RESEMBLING  CANCER,     (x  10.) 

From  a  man  thirty- two  years  old  who  died  of  Bright' s  disease  and  organic  disease  of 
the  heart,  a  is  the  spot  like  cancer,  and  a  portion  of  it  is  represented  more  highly  magni- 
fied by  Fig.  119.  b  is  an  area  in  the  medullary  portion  which  shows  fibroid  disease. 
The  general  character  of  the  cortical  portion  is  similar  to  that  of  Fig.  109. 


THE   KIDNEY.  143 

contraction  of  the  kidney  begins  by  thickening  of  the  capsule  and  a 
depression  of  the  surface  of  the  organ  with  the  growth  of  fibrous  tissue 
beneath  has  already  been  mentioned,  and  the  process  illustrated  by 
Figs.  1 06  and  109,  and  it  was  stated  that  such  is  the  commonest  mode 
of  origin  of  the  disease.  My  studies,  however,  have  led  me  to  believe 
that  fibrosis  in  some  exceptional  instances  begins  in  the  medullary 
portion.  Occasionally  at  post-mortem  examinations  the  cones  will  be 
found  to  be  very  light-colored,  almost  whitish,  so  that  they  present  a 
very  strong  contrast  in  color  with  the  rest  of  the  kidney,  and  at  the 
same  time  they  are  very  hard  to  the  touch.  Several  times  when  I 
have  examined  such  tissue  with  the  microscope  I  have  thought  the 
amount  of  epithelium  less  than  normal  and  the  fibrous  tissue  increased, 
and  yet  there  was  no  discoverable  disease  of  the  cortex.  Such  a 
condition  is  difficult  to  be  sure  of,  for  the  change  is  not  a  gross  one, 
and  it  would  be  still  more  difficult  to  demonstrate.  However,  as  the 
macroscopic  appearances  and  the  result  of  microscopical  examination 
point  in  the  same  direction,  I  have  been  led  to  believe  that  sometimes 
fibrosis  of  the  kidney  begins  in  the  medullary  tissue. 

Fig.  119  represents  a  portion  of  the  growth  resembling  cancer,  the 
whole  of  which  is  included  under  less  amplification  in  Fig.  118.  (See 
description  of  Fig.  118.)  It  has  already  been  said  that  the  case  was 
one  of  Bright's  disease  and  heart  disease  in  a  man  of  thirty-two.  The 
patient  died  having  dropsy  and  dyspnoea  and  a  typical  development 
of  all  the  symptoms  which  are  common  to  such  a  condition.  At  the 
post-mortem  examination  there  was  nothing  found  resembling  cancer 
except  the  one  minute  spot  in  the  kidney,  nor  did  the  microscope 
reveal  the  existence  of  anything  of  the  kind,  although  sections  of  the 
heart,  aorta,  lungs,  liver,  and  spleen,  as  well  as  of  the  kidney,  were  ex- 
amined. The  drawings  show  so  far  as  concerns  the  growth  a  condi- 
tion of  affairs  foreign  to  contraction  of  the  kidney,  of  which  the  case 
was  a  typical  instance.  The  growth  is  seen  in  the  low-power  picture 
to  be  a  little  more  than  one  millimetre  across,  and  sections  of  it  were 
made  in  more  than  one  direction,  which  showed  it  to  be  spherical. 
There  is  a  distinct  wall  around  it  separating  it  from  the  renal  tissue. 
The  high-power  drawing  shows  the  details  of  structure :  its  capsule  is 
formed  of  fibrous  tissue,  and  from  it  spring  cauliflower-like  growths 
composed  of  a  fibrous  stem  with  columnar  cells  arranged  upon  each 
side.  Other  similar  fragments  lie  loosely  in  the  central  mass.  These 
also  probably  grew  from  the  fibrous  capsule,  but  were  separated  from 
it  in  cutting  the  section.  The  general  mass  of  the  central  portion  of 


144  THE   ORIGIN   OF   DISEASE. 

the  growth  is  composed  of  cells  and  fibrous  shreds  which  are  so  de- 
generated in  many  places  as  to  have  no  distinct  outlines.  According 
to  accepted  pathological  classifications,  the  growth  must  be  placed 
with  the  neoplasms,  for  such  tissue  is  not  known  to  have  a  natural 
home  in  the  kidney,  and  the  cauliflower  growths  springing  from  the 
fibrous  capsule  are  strikingly  like  some  forms  of  cancer.  An  easy 
escape  from  the  difficulty  of  explaining  what  the  growth  really  was 
and  how  it  arose  is  to  assume  that  it  was  cancer,  and  that  others  of 
similar  nature  existed  in  the  body  of  the  patient,  but  were  not  found 
for  lack  of  sufficient  search,  or  that  this  was  the  beginning  of  cancer 
and  if  the  patient  had  lived  a  little  longer  it  would  have  shown  its  well- 
known  malignant  nature  by  the  enlargement  of  the  primary  growth 
and  the  development  of  secondary  growths.  Such  an  assumption  is 
not  warranted  by  the  facts.  Among  surgeons  of  large  experience 
there  have  always  been  many  who  believe  that  a  blow  may  be  the 
determining  cause  of  cancer  of  the  breast  in  a  woman,  or  the  excessive 
use  of  a  pipe  of  cancer  of  the  lip  or  tongue.  On  the  other  hand,  it 
is  generally  accepted  as  a  fact  that  cancer  is  in  some  way  of  a  spe- 
cific nature  and  that  its  spread-  is  due  to  an  infectious  quality, — that 
the  metastases  are  due  to  infection  of  the  more  distant  parts  by  the 
primary  tumor  which  is  assumed  to  be  the  centre  from  which  all  the 
other  growths  arise,  and  to  be  their  cause.  The  beliefs  that  cancer 
can  be  induced  by  an  irritant  or  by  injury  and  that  it  is  a  specific 
disease  of  an  infectious  nature  are  irreconcilable.  To  say  that  some 
individuals  are  of  such  nature  that  their  bodies  present  a  fertile  soil 
in  which  the  specific  seed  of  cancer  will  grow  readily  while  others  are 
sterile  is  to  drive  too  far  the  parallel  with  agricultural  conditions.  It  is 
well  known  that  many  plants  which  will  flourish  in  one  soil  will  hardly 
germinate,  much  less  grow,  in  others,  but  this  homely  agricultural 
truth  has  been  used  to  explain  difficulties  and  to  overcome  irrecon- 
cilable facts  in  human  pathology  until  it  is  difficult  to  hear  it  with 
patience.  To  accept  it  in  regard  to  cancer  it  is  necessary  to  believe 
that  in  those  capable  of  having  the  disease  the  seed  must  always  be 
lurking  in  the  system,  ready  to  break  out  as  soon  as  the  requisite 
irritation  is  supplied.  It  involves  the  assumption  in  the  first  place  of 
the  specific  and  infectious  nature  of  cancer,  that  it  is  of  extraneous 
nature,  a  something  that  attacks  the  body  from  without,  and  that  it 
can  in  no  wise  be  due  to  deformity  or  misdirected  growth  of  the 
natural  tissues.  Such  a  method  of  inference  is  that  of  the  weak  or 
specious  logician  who,  having  assumed  his  premises,  proceeds  to  draw 


FIG.  119.— GROWTH  IN  THE  KIDNEY  RESEMBLING  CANCER,     (x  105.) 

Part  of  the  region  a  in  Fig.  118,  more  highly  magnified,  c  is  the  fibrous  capsule  which 
surrounds  the  growth.  To  the  left  of  this  is  the  new  growth,  and  to  its  right  fibrous  renal 
tissue,  /"is  a  fibroid  Malpighian  body,  and  about  it  is  the  fibrous  renal  tissue,  showing 
much  round-cell  infiltration.  In  the  new  growth,  d  denotes  a  cauliflower  excrescence 
which  springs  from  the  fibrous  capsule,  and  e  a  loose  shred  of  organized  tissue,  d  and  c 
are  of  similar  structure,  being  composed  of  a  central  fibrous  strand  with  columnar  cells 
set  upon  both  sides.  They  much  resemble  some  of  the  forms  of  epithelial  cancer. 


FK;.  119. 


THE   KIDNEY.  145 

conclusions  without  stopping  to  ascertain  that  the  premises,  which 
are  the  foundation  of  the  structure,  are  correct.  The  theory  is  so 
complicated,  and  involves  so  much  that  cannot  be  explained  by  the 
laws  governing  the  growth  of  vegetables,  from  which  the  simile  of  the 
fertile  soil  was  derived,  that  one  is  warranted  in  declining  to  accept  it. 
In  the  discussion  of  lesions  of  the  blood-vessels  it  has  already  been 
shown  (Fig.  38)  that  growths  are  sometimes  found  in  the  walls  of 
vessels  presenting  some  of  the  physical  characteristics  of  cancer  but 
which  certainly  were  not  cancerous,  and  attention  was  called  to  the 
fact  that  in  the  skin  of  infants  the  epithelial  cells  often  arrange  them- 
selves in  whorls  which  are  similar  to  the  cell-nests  of  skin  cancer. 
These  two  instances  show  that  it  is  possible  for  the  cells  to  arrange 
themselves  in  such  a  way  as  to  produce  an  imitation  of  cancer.  It  is 
much  more  reasonable  to  believe  that  the  tumor  in  the  kidney  was  the 
result  of  misdirected  cell-growth  and  that  it  imitated  cancer  than  to 
believe  that  it  was  cancerous. 

Fig.  1 20  is  from  the  kidney  of  a  woman  sixty-one  years  old  who 
died  of  dysentery  and  Bright's  disease.  The  capsule  is  very  thick, 
the  tubules  are  somewhat  dilated,  and  the  epithelium  is  degenerated, 
having  lost  its  sharpness  of  outline  and  characteristic  columnar  ap- 
pearance. The  purpose,  however,  for  which  the  drawing  was  made 
was  to  show  the  condition  of  three  Malpighian  bodies,  which  are 
included  and  which  demonstrate  increasing  gradations  of  fibrosis. 
(See  description.)  In  the  one  least  diseased  Bowman's  capsule  is  very 
much  thickened,  the  thickening  being  of  the  inner  surface  and  having 
occurred  in  such  a  way  as  to  reduce  the  space  for  the  capillary  loop, 
which  is  still  very  distinct,  although  not  more  than  one-third  the 
natural  size.  Outside  of  Bowman's  capsule  there  is  an  area  of  round- 
cell  infiltration,  which  denotes  that  inflammation  constituted  a  part 
of  the  process  of  fibrosis.  At  this  stage  the  Malpighian  body  is  of 
normal  size,  being  about  two-tenths  of  a  millimetre  in  diameter.  The 
Malpighian  body  in  the  second  stage  of  fibrosis  is  reduced  in  size  by 
about  one-fourth,  being  between  one-tenth  and  two-tenths  of  a  milli- 
metre in  diameter.  Its  Bowman's  capsule  is  of  the  same  degree  of 
thickness  as  the  first  one,  but  the  space  for  the  capillary  loop  is  smaller, 
and  the  loop  itself  is  no  longer  recognizable  as  a  capillary,  being  re- 
duced to  a  mere  ball  of  fibrous  tissue  of  slightly  different  appearance 
from  Bowman's  capsule,  with  which  it  is  in  contact.  The  body  is 
surrounded  by  an  area  of  round-cell  infiltration  which  is  much  more 
extensive  than  that  around  the  first  one.  In  the  third  stage  of  fibrosis 

10 


146  THE   ORIGIN   OF   DISEASE. 

the  Malpighian  body  has  entirely  lost  its  character,  and  is  nothing  but 
a  little  fibrous  ball  which  is  only  one-tenth  of  a  millimetre  in  diameter, 
and  therefore  reduced  in  size  by  one-half.  It  is  not  even  surrounded 
by  an  area  of  inflammation.  If  these  three  Malpighian  bodies  consti- 
tute a  type  of  fibroid  destruction,  the  process  consists  of  thickening 
of  Bowman's  capsule  and  inflammation  of  the  surrounding  tissue.  In 
this  process  of  disease  the  capillary  loop  does  not  appear  to  take  any 
very  active  part,  although  in  the  second  stage  it  has  been  converted 
into  a  fibrous  mass  which  was  probably  entirely  impermeable  to  the 
passage  of  blood.  Inflammation  is  considerable  in  the  first  stage,  is 
still  more  extensive  in  the  second,  and  has  almost  entirely  faded  away 
in  the  third. 

Fig.  121  shows  a  condition  of  the  capsule  of  the  kidney  which  is 
common  and  characteristic  of  renal  fibrosis.  The  section  is  from  a 
man  of  forty-eight  who  died  of  dysentery  and  had  fibroid  and  cystic 
disease  of  the  kidneys.  A  casual  glance  at  the  drawing  might  lead 
one  to  say  that  it  represents  renal  tissue  and  an  unnaturally  thin  cap- 
sule with  perirenal  fat  adherent  to  it.  Exactly  the  contrary,  how- 
ever, is  the  real  explanation  of  the  appearances  :  the  capsule  is  greatly 
thickened,  and  its  layers  have  been  torn  apart  so  as  to  form  wavy  lines 
and  cavities.  Some  of  the  cavities  are  circular,  and  they  resemble  to 
a  limited  extent  fat  cells.  A  moment's  consideration,  however,  should 
be  sufficient  to  satisfy  any  one  that  the  tissue  is  not  fat.  The  cavities 
are  larger  than  ordinary  fat  cells,  and  the  fibrous  tissue  and  its  arrange- 
ments are  such  as  to  make  it  certain  the  material  is  not  fat.  Perirenal 
fat  is  not  very  different  from  other  forms  of  fat,  and  an  example  of  its 
appearance  is  exhibited  by  Fig.  no,  which,  however,  is  not  typical, 
as  it  is  more  fibroid  than  natural.  The  irregular  cavities  and  thick 
shreddy  fibrous  material  shown  in  the  drawing  suggest  the  explana- 
tion that  some  liquid  or  semi-solid  material  had  been  effused  into  the 
substance  of  the  capsule  and  had  forced  its  parallel  layers  apart.  As 
already  said,  this  condition  of  the  capsule  is  common  in  fibroid  kidney, 
and  its  existence  gives  rise  occasionally  to  a  curious  anomaly.  It  is 
well  known  that  generally  in  cases  of  fibroid,  and  especially  in  granular 
kidney,  when  the  surface  is  uneven  the  capsule  is  more  tightly  ad- 
herent than  natural.  A  peculiar  condition  in  cases  of  granular  kidney 
is  that  it  often  seems  nearly  impossible  to  remove  the  kidney  from  the 
body  with  the  capsule  still  upon  it.  Careful  investigation  in  such  in- 
stances has  revealed  that  the  whole  of  the  capsule  was  not  pulled  off, 
but  that  a  thin  layer  of  it,  as  is  shown  in  the  drawing,  remained  ad- 


FIG.  120.— FIBROID  KIDNEY,     (x  50.) 

From  an  elderly  woman  who  died  of  dysentery  and  Bright' s  disease,  c  is  the  capsule, 
which  is  very  thick  ;  h  is  a  loose  shred  of  capsule  ;  d,  e,  and  f  are  Malpighian  bodies  in 
different  stages  of  fibrous  destruction,  d  has  a  leaf-shaped  remnant  of  the  capillary  loop 
and  a  thick  fibrous  capsule,  e  has  at  its  centre  a  remnant  of  the  capillary  loop  which  is 
surrounded  by  the  thickened  fibrous  capsule  of  Bowman,  f  is  a  small  fibroid  ball.  All 
three  are  surrounded  by  areas  of  round-cell  infiltration. 

FIG.  121. — SHREDDED  AND  THICKENED  CAPSULE  OF  KIDNEY.     (X  50.) 

From  a  man  of  forty-eight  years  who  died  of  dysentery.  The  layers  of  the  capsule 
have  been  torn  apart  by  liquid  which  filled  the  apparently  empty  spaces.  It  is  impossible 
to  suppose  this  was  fatty  change,  for  Fig.  no  shows  perirenal  fat,  and  the  contrast  in 
appearance  is  very  great. 


VlC,.    121. 


THE   KIDNEY.  147 

herent  to  the  kidney.  This  effect  is  due  to  the  separation  of  the 
capsule  into  two  layers,  the  thicker  of  which  is  torn  off  with  the 
perirenal  fat,  leaving  a  thin  layer  upon  the  kidney.  To  the  naked 
eye  it  appears  as  if  none  of  the  capsule  is  left,  and  only  microscopical 
examination  demonstrates  the  fact  that  a  part  of  it  remains  adhering 
to  the  kidney. 

In  no  other  organ  of  the  body  are  cysts  known  to  be  so  common 
as  in  the  kidney,  and  the  characteristics  of  renal  cysts  have  there- 
fore been  very  closely  studied.  Although  such  is  the  case,  there 
remains  a  great  deal  to  be  learned  in  regard  to  them,  and  even  yet 
there  is  much  difference  of  opinion  about  some  of  their  peculiarities. 
It  has  sometimes  been  said  that  cysts  in  the  kidneys  of  the  aged  are 
not  under  all  circumstances  to  be  considered  as  evidence  of  disease. 
Such  a  belief  has  always  seemed  to  me  as  untenable  as  would  be  the 
position  of  one  who  should  assert  that  cavities  in  the  lungs  are  not 
always  to  be  attributed  to  disease.  Renal  cysts  must  under  all  cir- 
cumstances be  either  congenital  or  due  to  disease  which  has  destroyed 
portions  of  the  kidneys  to  make  room  for  the  cysts. 

Fig.  122  represents  a  cyst  of  the  kidney  from  a  man  of  fifty-two 
who  died  of  organic  heart  disease.  The  cyst  lies  directly  beneath  the 
capsule,  and  across  it  are  a  number  of  lines,  some  of  which  are  com- 
plete, crossing  the  cavity  from  side  to  side,  while  others  reach  only 
part  way  across.  These  lines,  for  as  such  they  appear  when  seen 
in  section,  are  portions  of  partitions  and  shelves  which  divided  or 
partially  divided  the  cyst-cavity.  The  cavity  of  the  cyst  was  there- 
fore composed  of  a  number  of  chambers,  some  of  which  were  com- 
pletely separated  from  one  another,  or  again  the  chambers  communi- 
cated because  they  were  only  partially  separated  by  shelves.  It  is  an 
exceedingly  common  characteristic  of  cysts  of  the  kidney  to  be  sub- 
divided as  shown  by  the  drawing.  The  partitions  when  seen  with  the 
naked  eye  appear  as  thin  membranes  of  delicate  texture.  If  there  is 
one  particular  in  regard  to  which  cysts  differ  more  than  another,  it  is 
in  the  nature  of  their  walls.  In  the  cyst  under  consideration  the 
cavity  was  hollowed  out  of  the  renal  tissue  directly,  and  there  is  no 
differentiated  wall,  but  the  cyst-contents  lay  in  contact  with  the  kidney 
tissue.  This  is  shown  by  the  drawing,  but  is  made  even  more  striking 
by  Fig.  123,  which  is  an  enlarged  picture  of  a  portion  of  the  same 
tissue  more  highly  magnified.  In  it  there  is  no  trace  of  anything  like 
a  fibrous  cyst-wall.  A  Malpighian  body  is  included  which  lay  in  one 
of  the  partitions.  The  Bowman's  capsule  of  this  is  somewhat  thick- 


148  THE   ORIGIN   OF   DISEASE. 

ened,  but  the  capillary  loop  remained  in  a  fairly  good  state  of  preser- 
vation. The  cells  forming  one  of  the  shelves  are  very  like  some  cells 
which  have  already  been  depicted  as  existing  in  the  wall  of  a  cyst  of 
the  spleen.  There  is  every  reason  to  suppose  that  these  cells  which 
are  so  unlike  the  ordinary  columnar  secreting  cells  lining  most  of 
the  renal  secreting  tubules  have  simply  been  modified  by  their  changed 
conditions  and  surroundings,  and  that  there  has  not  been  anything 
like  a  new  growth. 

Fig.  124  is  from  the  kidney  of  a  man  of  about  sixty  who  died  of 
illuminating-gas  poisoning  and  was  found  to  have  pulmonary  phthisis 
and  cystic  disease  of  the  kidneys.  The  drawing  is  of  a  portion  of 
tissue  bounding  a  cyst,  and  it  shows  that  the  cyst-wall  is  composed  of 
a  thick  layer  of  fibrous  tissue.  The  renal  tissue  adjacent  to  the  cyst- 
wall  is  fibroid,  there  being  Malpighian  bodies  which  have  been  con- 
verted into  mere  fibrous  balls,  and  others  around  which  the  capsule  of 
Bowman  is  fibroid  and  thicker  than  natural.  Throughout  the  whole 
of  the  tissue  there  has  been  a  growth  of  fibrous  material  to  such  an 
extent  that  were  it  not  for  the  Malpighian  bodies  it  could  hardly  be 
recognized  as  kidney.  The  contrast  between  this  picture  and  the  pre- 
ceding is  very  striking  in  that  the  one  cyst  has  such  a  distinct  fibrous 
wall  and  the  other  is  a  cavity  hollowed  out  of  the  tissue.  It  is  strange 
that  it  should  be  possible  for  cysts  to  differ  so  far,  although  there  is 
every  reason  to  suppose  the  process  is  the  same  in  the  two  cases, 
the  presence  or  absence  of  a  fibrous  cyst-wall  signifying  only  variation 
caused  by  difference  of  the  circumstances  under  which  the  cyst  grew 
and  the  condition  of  the  tissue. 

Fig.  125  represents  diseased  kidney  which  is  interesting  for  more 
than  one  reason.  The  case  was  one  of  hydronephrosis  in  which  the 
kidney  was  almost  entirely  destroyed.  Nothing  is  known  of  the  history 
of  the  patient.  There  are  four  good-sized  cavities,  a  larger  one  and 
below  it  three  smaller  ones,  which  it  would  seem  can  be  classified  only 
as  cysts.  All  the  cavities  are  nearly  filled  with  structureless  solid  ma- 
terial, and  the  walls  are  formed  of  cells  like  those  of  epithelium.  Scat- 
tered through  the  tissue  are  numerous  renal  tubules  containing  casts. 
The  cysts  and  tubules  are  similar  in  all  respects  except  size ;  the  cyst- 
contents  and  the  casts  in  the  tubules  are  alike,  and  the  cells  of  both 
present  the  same  appearance.  These  cells  are  little  like  healthy  renal 
epithelium,  but  the  situation  they  occupy  shows  that  they  certainly  are 
renal  secreting  cells.  Their  appearance  is  almost  exactly  the  same  as 
that  of  some  of  the  cells  in  Fig.  123,  which,  however,  are  twice  as 


FIG.  122. —RENAL  CYST  WITHOUT  FIBROUS  WALL,     (x  6.) 

From  a  man  of  fifty-two  years  who  died  of  organic  heart  disease,  c  is  the  capsule. 
The  cyst  is  large,  irregularly  shaped,  and  directly  underneath  the  capsule.  Across  it  pass 
several  lines.  These  lines  are  parts  of  membranes  which  formed  shelves  and  partitions 
irregularly  dividing  the  cyst  into  separate  or  partly  separate  chambers.  The  cyst-cavity 
contains  some  amorphous  material  and  loose  shreds,  d  denotes  the  region  shown  more 
highly  magnified  by  Fig.  123.  At  d  is  a  Malpighian  body  almost  uncovered  in  the  cyst- 
cavity.  There  is  nowhere  any  differentiated  cyst-wall ;  the  contents  of  the  cyst  lay  di- 
rectly in  contact  with  the  kidney  tissue. 

FIG.  123.— RENAL  CYST  WITHOUT  FIBROUS  WALL,     (x  105.) 

The  region  d'vn.  Fig.  122,  more  highly  magnified.  The  same  relative  position  has  been 
maintained.  The  Malpighian  body  is  here  b,  and  it  is  seen  to  form  part  of  one  of  the 
shelves  (lines)  seen  in  Fig.  122.  e  and  f  are  in  the  cyst-cavity,  and  c  indicates  a  part  of 
one  of  the  shelves  in  which  the  cells  are  large  and  oval.  It  looks  like  kidney  tissue 
altered  by  its  changed  surroundings.  The  cells  at  c  closely  resemble  those  shown  as  form- 
ing the  wall  of  a  cyst  in  the  spleen  in  Figs.  96,  97,  and  98.  There  is  nowhere  any  fibrous 
cyst- wall,  kidney  tissue  forming  the  boundary  of  the  cyst,  a  is  an  arteriole  with  thickened 
fibrous  walls. 


FIG.  122. 


FIG.  123. 


tmot 


FIG.  124. — RENAL  CYST  WITH  THICK  FIBROUS  WALL,     (x  105.) 

From  a  man  of  about  sixty  years  who  had  phthisis  and  cystic  kidneys  and  died  of  illumi- 
nating-gas poisoning.  The  drawing  is  of  a  portion  of  the  wall  of  a  renal  cyst,  and  is  to 
be  contrasted  with  Fig.  123.  Between  /  and  g  is  the  thick  fibrous  membrane  which 
formed  the  wall  of  the  cyst,  h  is  placed  in  the  cyst-cavity.  The  renal  tissue  is  fibroid, 
and  there  is  round-cell  infiltration. 


FIG.  124. 


h 


THE   KIDNEY.  149 

much  magnified.  The  disease  is  to  be  explained  only  as  an  early 
stage  of  cystic  degeneration.  Whether  such  dilated  tubules  would 
have  undergone  further  enlargement,  thus  forming  the  ordinary  cysts 
which  are  of  such  frequent  occurrence,  cannot  be  known.  Cavities 
like  those  described  are  not  rare  in  cases  of  extreme  contraction,  and 
there  were  a  good  many  of  them  in  the  kidney  represented  by  Fig. 
1 14,  but  the  amplification  used  in  making  the  picture  was  not  suffi- 
cient to  show  them.  At  the  stage  under  consideration  the  cysts  are 
always  filled  with  structureless  solid  material,  which,  as  has  been  said, 
appears  to  be  exactly  like  the  casts  in  the  undilated  secreting  tubules. 
It  is  not  unlikely  that  the  growth  of  the  casts  has  something  to  do 
with  the  production  of  the  cysts.  If  such  dilated  tubules  as  those  de- 
picted, which  have  grown  so  much  larger  than  natural  that  they  are 
correctly  classified  as  cysts,  ever  develop  into  ordinary  cysts,  they 
must  undergo  great  modification.  Ordinary  cysts,  as  has  been  shown, 
sometimes  have  fibrous  walls  and  again  have  no  differentiated  walls, 
and  they  generally  contain  a  clear  thin  fluid,  although  sometimes 
there  is  semi-solid  material  in  them.  Cysts  such  as  those  shown  by 
the  drawing,  which  by  their  appearance  still  clearly  demonstrate  their 
origin  in  dilatation  of  the  tubules,  are  always  filled  with  solid  material 
like  casts,  and  have  a  boundary  of  epithelial  cells,  which,  however, 
have  been  so  modified  as  to  have  lost  all  resemblance  to  healthy 
kidney  epithelium. 

Fig.  125  presents,  besides  the  cystic  dilatations  of  the  tubules  which 
have  been  under  discussion,  other  peculiarities  which  are  of  great  in- 
terest. There  are  two  amyloid  arterioles,  and  the  capsule,  which  is 
thick,  has  been  thrown  into  wavy  folds  and  has  a  homogeneous  glassy 
appearance  like  amyloid  material.  This  latter  condition  is  not  shown 
so  well  by  the  drawing  as  might  be  desired,  for  it  is  impossible  to 
produce  the  effect  with  pen  and  ink,  but  the  section  itself  is  most 
striking.  The  arterioles  are  exactly  like  the  vessel  represented  in 
Fig.  126,  which  is  in  all  respects  a  typical  example  of  amyloid  disease. 
It  is  singular  that  in  a  case  of  hydronephrosis  there  should  be  amyloid 
disease  of  the  blood-vessels  and  this  peculiar  condition  of  the  thick 
and  fibrous  capsule  of  the  kidney,  which  I  believe  is  only  another 
form  of  amyloid  change.  The  case  was  in  no  way  one  which  would 
ordinarily  be  classed  as  of  amyloid  disease.  It  has  so  frequently 
happened  to  me,  however,  in  cases  of  chronic  disease  of  the  kidney 
involving  extensive  growth  of  morbid  fibrous  tissue,  to  find  more  or 
less  of  this  homogeneous  glassy  material,  which  when  it  exists  in 


150  THE   ORIGIN  OF  DISEASE. 

large  deposits  is  named  amyloid  degeneration  and  is  supposed  to 
be  the  result  of  a  special  process  of  disease,  that  I  have  been  driven 
to  the  belief  that  amyloid  deposit  is  only  a  form  of  fibrous  tissue 
in  which  there  are  few  nuclei  and  great  quantities  of  structureless 
substance. 

Fig.  126  is  from  a  section  typical  of  amyloid  disease  of  the  kidney, 
and  its  appearances  lend  support  to  the  foregoing  explanation  of  amy- 
loid degeneration.  When  portions  of  any  of  the  organs  are  destroyed 
by  chronic  disease  the  natural  tissue  is  to  some  extent  replaced  by 
fibrous  tissue.  Morbid  fibrous  tissue  is  not  exactly  like  healthy 
fibrous  structures,  and,  being  the  result  of  a  destructive  process,  it  is 
hardly  to  be  expected  that  it  should  be.  It  differs  so  much  at  different 
times  and  under  differing  circumstances  as  to  make  it  seem  unreason- 
able to  call  it  always  by  the  one  name  of  morbid  fibrous  tissue,  and 
yet,  upon  closer  consideration,  even  when  two  varieties  of  it  seem 
most  dissimilar  it  is  impossible  to  avoid  the  conclusion  that  it  is  the 
same  thing.  Morbid  fibroid  tissue  may  grow  in  the  liver,  spleen,  or 
kidney  in  a  manner  so  latent  that  no  change  is  at  any  time  discover- 
able except  an  increase  of  the  fine,  nearly  structureless  framework 
of  the  organ.  There  may  be  no  apparent  activity  of  life  in  the  af- 
fected part  and  no  new  growth  of  cells,  but  the  process  goes  on  until 
there  are  large  bands  of  fibrous  material  poor  in  nuclei  running 
through  the  tissue,  destroying  part  of  it  to  make  room  for  themselves. 
Such  is  the  latent  form  of  fibrosis.  On  the  other  hand,  when  irritation 
and  inflammation  are  active,  any  of  the  tissues  may  be  so  over- 
whelmed by  infiltration  as  to  be  unrecognizable  and  appear  as  a  con- 
fused and  crowded  mass  of  the  round  cells  of  inflammation.  These 
two  extreme  forms  of  fibrosis,  the  bands  of  almost  structureless  fibrous 
tissue  poor  in  nuclei,  and  the  areas  of  round-cell  infiltration,  are  so 
different  that  at  first  sight  it  is  difficult  to  believe  they  can  even 
be  related,  much  less  only  varieties  of  the  same  disease.  In  the  case 
of  round-cell  infiltration,  however,  if  the  disease  goes  on,  and  sup- 
puration does  not  ensue,  time  will  reduce  the  inflammation.  As  this 
becomes  less  active,  the  cells  disappear,  and  their  place  is  taken  by 
fibrous  tissue.  As  the  cells  become  fewer  and  the  fibrous  or  struc- 
tureless material  increases,  it  is  evident  that  through  the  process  of 
inflammation  with  its  cell  activity  the  same  goal  is  reached,  the  de- 
struction of  the  natural  tissue  of  the  organ  and  its  replacement  by 
morbid  fibrous  tissue.  Both  roads  lead  to  the  same  end,  the  forma- 
tion of  common  morbid  fibrous  tissue. 


FIG.  125.— SMALL  RENAL  CYSTS  AND  AMYLOID  DISEASE.     (X  50.) 

From  a  case  of  hydronephrosis.  The  kidney  was  atrophied  and  so  changed  that  it  was 
almost  beyond  recognition.  The  drawing  includes  the  whole  depth  of  the  thickened  cap- 
sule and  tissue  beneath.  There  is  a  good-sized  cyst  adjacent  to  the  capsule,  and  directly 
beneath  it  are  three  smaller  ones.  All  the  cysts  contain  structureless  solid  material,  and 
around  this  in  each  instance  is  a  complete  circle  of  cells  unlike  the  epithelium  of  renal 
tubules,  t  is  a  tubule  containing  a  cast,  and  there  are  many  others  of  similar  nature  near 
it.  These  tubules  containing  casts  are  almost  exactly  like  the  cysts  except  in  size.  The 
cells  both  of  the  tubules  and  of  the  cysts  are  unlike  healthy  renal  epithelium.  Much  of 
the  tissue  included  in  the  drawing  is  fibrous,  and  it  is  doubtful  if  any  of  it  could  have 
been  recognized  as  kidney  from  its  appearance  alone,  so  greatly  has  the  disease  changed 
it.  a,  a  are  two  minute  arterioles  with  walls  thick  and  homogeneous,  and  their  calibres 
small ;  they  are  exactly  like  amyloid  vessels,  g  is  the  lower  border  of  the  capsule.  The 
capsule  is  thickened  and  of  peculiar  structure,  being  thrown  into  wavy  lines  and  having 
a  homogeneous  glassy  appearance  like  amyloid  deposit.  This  glassy  tone  cannot  be  very 
well  shown  in  a  pen-and-ink  drawing. 

FIG.  126. — AMYLOID  ARTERIOLE  AND  MALPIGHIAN  BODIES  OF  THE  KIDNEY,    (x  50.) 

From  a  section  of  amyloid  kidney.  Nothing  is  known  of  the  patient,  y  includes  an 
amyloid  arteriole  (a)  and  an  amyloid  Malpighian  body,  both  being  surrounded  by  fibrous 
and  infiltrated  tissue,  z  is  another  amyloid  Malpighian  body.  Its  Bowman's  capsule 
is  thickened  and  fibrous,  and  outside  of  it  the  tissue  is  fibrous  and  infiltrated.  In  this 
Malpighian  body  the  various  turns  of  the  capillary  loop  are  still  distinct,  while  in  y  the 
capillary  has  melted  into  an  almost  even  amyloid  mass.  The  structure  of  this  typical 
amyloid  deposit,  both  of  the  Malpighian  capillaries  and  of  the  arteriole  (a),  is  very  like 
some  material  in  the  foregoing  picture,  and  in  the  ileum  represented  by  Figs.  104  and  105. 


FIG. 


FIG.  126. 


THE   KIDNEY.  151 

In  what  respect  is  the  amyloid  deposit  different  from  some  of  the 
forms  of  morbid  fibrous  tissue  ?  It  does  not  seem  reasonable  that  it 
should  be  given  a  name  for  itself  and  be  supposed  to  be  a  heteroge- 
neous product  in  the  body  simply  because  it  turns  brown  when  stained 
with  iodine.  There  is  nothing  in  the  appearance  of  Fig.  126,  either  in 
the  Malpighian  bodies  or  in  the  arteriole,  which  is  not  more  satisfac- 
torily explained  as  being  due  to  fibrous  growth  than  by  the  assump- 
tion that  some  new  and  heterogeneous  material  was  deposited  in  the 
walls  of  the  Malpighian  capillary  and  of  the  arteriole.  There  is  a 
general  great  excess  of  the  fibrous  tissue  of  the  kidney,  besides  the 
changes  in  the  arterioles  and  Malpighian  bodies,  and  this  is  always  the 
case  in  amyloid  disease,  general  fibrosis  of  the  organ  affected  being  as 
much  a  part  of  the  process  as  the  deposit  of  the  amyloid  material 
itself. 

Before  dismissing  the  subject  of  the  kidney,  some  points  which 
have  not  yet  been  touched  upon  must  be  brought  out,  and  certain 
relations  to  one  another  of  disease  conditions  already  mentioned  must 
be  noticed.  In  what  has  been  heretofore  said  it  has  been  my  inten- 
tion to  emphasize  the  fact  that  of  all  diseases  of  the  kidney  there  is 
none  so  common  and  therefore  none  so  important  as  fibrosis.  Fi- 
brosis is  as  inevitable  to  age  as  wrinkles  of  the  skin,  and  its  extent 
and  distribution  have  great  influence  upon  acute  diseases,  because 
fibroid  organs  are  much  more  liable  to  inflammation  than  healthy 
tissue.  Three  different  phases  of  fibrosis  of  the  kidney  are  demon- 
strated by  Figs.  109,  no,  and  112,  and  they  present  both  points  of 
resemblance  and  of  contrast.  There  are  other  varieties  of  the  disease, 
of  course,  besides  these  three,  and  some  such  are  exemplified  in  the 
series  of  illustrations.  The  essential  feature  is  the  production  of 
morbid  fibrous  tissue,  and  this  always  grows  at  the  expense  of  the 
natural  secreting  substance.  An  almost  invariable  accompaniment  is 
thickening  of  the  capsule  of  the  kidney,  and  with  it  unnatural  ad- 
hesion to  the  perirenal  fat.  In  cases  in  which  the  fibroid  deposit  is 
irregularly  distributed  there  are  generally  depressions  making  the 
surface  of  the  kidney  uneven.  Among  the  illustrations  are  included 
examples  of  each  of  these  lesions.  A  striking  peculiarity  of  fibrosis 
of  the  kidney — and  the  same  is  true  of  fibrosis  of  other  organs — is 
that  in  most  instances  it  seems  to  begin  near  the  surface,  the  capsule 
and  the  superficial  portion  of  the  kidney  being  first  involved.  Why 
this  should  be  so  is  not  at  present  understood,  but  that  such  is  the 
case  there  cannot  be  any  doubt.  To  return,  however,  to  the  three 


152  THE   ORIGIN   OF   DISEASE. 

illustrations.  In  Fig.  109  the  capsule  is  thick,  but  part  of  it  is  much 
thicker  than  the  rest,  and  is  depressed  below  the  general  level,  so  that 
there  was  a  pit  upon  the  surface  of  the  kidney.  Beneath  the  thickest 
and  depressed  portion  of  the  capsule  the  renal  tissue  has  lost  its 
ordinary  appearance  and  has  been  converted  into  a  mass  of  morbid 
fibroid  tissue,  which  is  rich  in  the  round  cells  of  inflammation  and  has 
scattered  through  it  a  few  shrunken  and  fibroid  Malpighian  bodies. 
From  this  diseased  region  beneath  the  capsule  fibroid  bands  extend 
in  various  directions  through  the  kidney.  The  tubules  are  dilated 
and  the  epithelial  cells  somewhat  degenerated,  but  most  of  the  kidney 
tissue  has  not  sustained  great  structural  change.  The  effect,  then,  of 
the  picture  is  of  kidney  the  greatest  part  of  which  is  composed  of 
natural  tissue,  but  through  which  ramify  fibrous  bands  which  in  their 
growth  destroyed  secreting  substance.  The  most  striking  feature, 
however,  is  that  it  looks  as  if  the  whole  morbid  fibrous  process  had 
had  its  origin  in  the  thick  and  depressed  portion  of  the  capsule  and 
subcapsular  fibroid  mass,  and  that  from  this  region  as  a  centre  the 
fibroid  tissue  had  grown  in  various  directions.  In  Fig.  no  also  the 
capsule  is  thick,  and  from  it  extend  fibrous  bands  into  the  perirenai 
fat,  which  contains  more  fibrous  tissue  than  healthy  fat.  The  appear- 
ance of  the  renal  tissue  itself  is  in  marked  contrast  with  that  last  de- 
scribed :  there  is  nothing  like  natural  epithelium  to  be  seen,  but  the 
tissue  presents  the  effect  of  a  smooth,  almost  structureless,  basis  ma- 
terial in  which  are  scattered  Malpighian  bodies  and  tubules,  some  of 
which  have  been  cut  lengthwise  and  others  across.  In  contrast  with 
the  previous  picture,  which  was  of  comparatively  healthy  kidney 
seamed  in  various  directions  by  disease,  this  one  is  everywhere  dis- 
eased, with  only  scattered  remains  of  the  natural  elements  in  it.  Fig. 
1 1 2  is  diseased  to  an  even  greater  degree,  for  if  it  were  not  for  the 
Malpighian  bodies  which  remain  it  could  not  be  recognized  as  kidney. 
The  capsule  is  thick,  as  in  both  the  others.  The  greatest  portion  of 
tissue  included  is  composed  of  heavy  fibrous  material,  rich  in  cells, 
and  through  this  are  scattered  open  spaces  formed  by  dilated  and 
broken  tubules.  Except  that  the  spaces  which  appear  empty  must 
have  been  filled  with  liquid  instead  of  air,  the  parallel  in  appearance 
and  mode  of  production  with  emphysema  is  exact.  It  is  impossible 
to  escape  from  the  conviction  that  the  process  is  the  same  in  lung 
and  in  kidney,  modified  by  the  differences  in  the  nature  of  the  tissue 
of  the  two  organs. 

Extensive  fibrosis  of  the  kidney  often  exists  and  yet  fair  or  even 


THE   KIDNEY.  153 

good  health  is  maintained.  This  must  be  because  while  portions 
of  the  kidney  are  destroyed  by  the  fibroid  growth  others  are  left  un- 
injured, and  it  explains  why  it  so  often  happens  that  in  persons  who 
have  died  of  other  causes  extensive  disease  of  the  kidney,  which  had 
not  been  suspected,  is  found  after  death.  As  has  been  already  said  in 
regard  to  other  organs,  it  is  probable  that  such  latent  disease  is  often 
in  some  way  the  determining  cause  of  acute  attacks.  When  such 
acute  attacks  terminate  fatally  the  antecedent  chronic  and  latent  dis- 
ease will  be  found  to  have  been  the  real  cause  of  death,  if  one  looks  a 
little  below  the  surface.  A  curious  feature  of  renal  fibrosis  which  is 
usually  associated  in  the  mind  with  the  thought  of  contraction  is  that 
the  kidney  may  be  of  the  natural  size  and  even  retain  its  ordinary 
weight  and  yet  be  exceedingly  fibroid.  If  such  a  kidney  be  cut  open  it 
will  be  seen  that  the  hilum  is  very  much  larger  than  natural  and  is 
filled  with  adipose  tissue,  while  the  renal  substance  which  lies  in  a 
semicircle  around  it  is  reduced  to  such  an  extent  that  perhaps  there  is 
not  more  than  one-half  the  normal  amount  of  it.  In  this  respect  the 
kidney  presents  a  parallel  to  a  certain  extent  with  what  is  so  well 
known  to  occur  in  the  liver  in  cases  of  hypertrophic  cirrhosis.  The 
difference,  however,  is  that  the  fibroid  liver  may  grow  to  be  very  much 
larger  and  heavier  than  natural,  while  the  utmost  that  the  kidney 
seems  able  to  attain  is  to  continue  of  normal  size  and  weight  when 
fibroid,  instead  of  shrinking.  It  has  been  said  that  fibrosis  is  most 
apt  to  begin  in  the  capsule  and  the  subcapsular  portions  of  the  kidney. 
When  the  disease  extends  from  this  region  it  more  frequently  passes 
down  the  pyramids  of  Ferrein,  which  include  the  straight  tubules  of 
the  cortex,  than  into  the  labyrinths. 

Degeneration  of  the  epithelium  is  more  often  seen  in  acute  disease 
of  the  kidney  than  in  the  chronic  forms,  and  when  it  is  extensive  in 
cases  of  slow  disease  like  fibrosis  it  is  the  result  of  an  acute  process 
engrafted  upon  the  chronic.  The  mode  of  its  destruction  varies  very 
much :  in  some  instances  the  lines  of  separation  of  cell  from  cell  dis- 
appear, and  the  nuclei  melt  away,  leaving  nothing  but  an  even  gran- 
ular mass  of  protoplasm,  while  in  others  the  protoplasm  is  destroyed 
and  the  cell  nuclei  are  left  in  so  good  a  state  of  preservation  that 
they  are  like  the  small  cells  which  are  so  abundantly  deposited  in 
inflamed  tissue. 

No  other  organ  produces  a  greater  variety  of  disease  of  the  blood- 
vessels than  the  kidney  when  it  is  fibroid.  Illustrations  of  such 
vessels  are  included  in  the  chapter  on  blood-vessels.  Fibrosis  of 


i54  THE   ORIGIN   OF   DISEASE. 

the  kidneys  is  so  often  found  in  persons  who  have  died  of  pulmonary 
phthisis  that  there  is  no  escape  from  the  conviction  that  the  processes 
are  related,  and  this  conviction  is  strengthened  when  it  is  recollected 
that  the  one  essential  of  both  diseases  is  the  production  of  morbid 
fibroid  tissue.  There  has  been  mentioned  in  this  chapter  an  iso- 
lated growth  which  was  found  in  the  kidney  in  a  case  of  Bright's  dis- 
ease which  presented  many  of  the  physical  characteristics  of  cancer, 
although  nothing  else  of  that  nature  was  discovered  at  the  post- 
mortem examination.  In  more  than  one  instance  it  has  happened  to 
me  to  find  in  cases  with  malignant  disease  of  the  kidney  that  there 
were  also  lesions  of  Bright's  disease  which  there  was  every  reason  to 
suppose  had  existed  in  the  kidney  before  the  malignant  disease.  Con- 
sideration of  the  life-history  of  cancer  makes  it  appear  that  the  theory 
of  its  extraneous  and  specific  nature  cannot  be  correct.  It  is  not  so 
well  known  by  physicians  as  it  should  be  that  extensive  fibrosis  of  the 
kidney  may  exist  and  yet  the  clinical  evidences  of  disease  be  entirely 
wanting.  The  most  striking  features  of  the  chronic  diseases  of  the 
kidney  which  have  been  under  consideration  are  that  they  are  all  so 
inextricably  commingled  that  to  attempt  to  separate  them  only  causes 
confusion,  and  makes  it  evident  that  there  is  really  only  one  disease, 
or  that  if  there  are  subdivisions  the  differences  are  slight  and  the 
processes  all  related,  and,  further,  that  old  age  always  brings  fibrosis, 
and  that  when  fibrosis  comes  early  it  is  like  age  in  youth. 


CHAPTER    XII. 

THE   SPINAL   CORD. 

THE  study  of  the  pathology  of  the  nervous  system  presents  greater 
difficulties  than  that  of  the  thoracic  and  abdominal  organs,  because 
of  the  great  complexity  of  nervous  diseases  and  the  delicacy  of  the 
tissue.  The  results  obtained  from  examination  of  the  spinal  cord  are 
satisfactory  because,  owing  to  its  cord-like  form,  a  complete  section 
across  any  part  of  it  can  be  made  and  submitted  to  microscopical  ex- 
amination. Any  disease,  therefore,  which  traverses  its  length  must 
be  discovered  if  only  a  single  section  is  thoroughly  studied.  This 
gives  a  certain  completeness  to  sections  of  the  cord.  It  must  be  con- 
fessed, however,  that  disease  is  more  frequently  found  at  different 
levels  than  extending  through  its  length.  The  conditions  in  other 
organs  are  very  different,  and  it  is  possible  only  to  select  minute  pieces 
hap-hazard  for  microscopical  examination  or  because  some  unnatural 
appearance  has  been  observed  with  the  unaided  eye.  Important  dis- 
ease for  this  reason  often  remains  undiscovered.  Most  diseases  of  the 
spinal  cord  are  to  be  recognized  only  by  the  use  of  the  microscope, 
being  undiscoverable  by  even  the  most  careful  examination  with  the 
unaided  eye.  There  are  few  spinal  diseases  which  produce  such  gross 
lesions  as  acute  meningitis,  in  which  sometimes  a  thick  layer  of  yellow 
plastic  lymph  may  be  found  within  the  dura  mater  entangled  in  the 
meshes  of  the  pia-arachnoid.  So  serious  a  lesion  as  a  complete  trans- 
verse myelitis  may  exist  and  escape  discovery  at  the  post-mortem  ex- 
amination, to  be  demonstrated  weeks  afterward  when  the  tissue  has 
been  prepared  and  sections  have  been  cut  for  microscopical  examina- 
tion. Some  years  ago  I  published  a  report  of  a  case  of  injury  of  the 
spinal  column,*  the  result  of  an  accident  at  sea,  in  which  no  evidence 
of  disease  was  discovered  at  the  post-mortem  examination.  Curious 
color-changes  indicative  of  lesions  were  evident  after  the  tissue  had 
been  for  some  time  in  preservative  fluid,  and  still  later  microscopical 
examination  revealed  the  presence  of  a  complete  transverse  myelitis 

*  A  Study  of  the  Paths  of  Secondary  Degeneration  in  a  Case  of  Injury  of  the  Cervical 
Spine,  by  Arthur  V.  Meigs.  American  Journal  of  the  Medical  Sciences,  August,  1890, 
and  Transactions  of  the  College  of  Physicians  of  Philadelphia,  March  5,  1890. 

155 


156  THE   ORIGIN   OF   DISEASE. 

and  extensive  disease  throughout  the  cord.  This  fact,  that  extensive 
disease  of  the  spinal  cord  may  exist  and  yet  escape  detection  unless 
searched  for  with  the  microscope,  it  is  very  important  to  keep  con- 
stantly in  mind,  for  it  emphasizes  the  necessity  for  thorough  examina- 
tion of  the  cord  in  all  cases,  although  there  may  be  a  priori  no  reason 
to  suppose  it  to  be  diseased.  In  the  chapters  dealing  with  other  organs 
it  is  pointed  out  that  frequently,  and  especially  in  persons  who  have 
died  of  chronic  disease,  lesions  are  found  of  latent  or  chronic  char- 
acter that  must  have  existed  long  before  the  attack  that  caused  death. 
It  will  be  shown  as  the  subject  of  the  pathology  of  the  spine  is  de- 
veloped that  this  is  the  case  with  it  as  much  as  with  any  of  the  other 
organs,  and  that  therefore  it  is  very  desirable  that  the  cord  should  be 
systematically  and  thoroughly  examined  in  all  the  forms  of  chronic 
disease.  This  I  have  tried  to  do,  but  have  succeeded  to  only  a  very 
limited  extent,  as  a  much  greater  amount  of  time  could  be  profitably 
spent  in  the  pursuit  of  such  a  study  than  the  duration  of  any  human 
life. 

The  greater  number  of  spinal  cords  I  have  examined  were  taken 
from  persons  who  died  of  diseases  during  the  course  of  which 
there  had  been  no  clinical  symptoms  indicating  involvement  of  the 
nervous  system,  and  yet  many  of  them  show  unmistakable  patho- 
logical lesions.  In  the  examination  of  nervous  tissues  it  is  necessary 
to  exercise  the  utmost  care  in  preserving  and  preparing  them  for 
microscopical  study,  so  that  changes  due  to  faulty  technique  shall  not 
be  mistaken  for  disease.  To  accomplish  this  some  uniform  method 
must  be  pursued  in  all  instances,  in  which  case  it  will  be  known,  after 
sufficient  experience  has  been  acquired  to  furnish  a  standard  of  or- 
dinary conditions,  that  any  unusual  appearances  must  be  the  result 
either  of  disease  or  of  post-mortem  changes.  In  addition  to  a  uniform 
method  of  examination  as  a  basis,  it  is  of  course  desirable  to  utilize 
other  methods  for  the  study  of  any  disease  discovered. 

It  is  remarkable  that  in  such  chronic  diseases  as  Bright's  disease, 
and  in  others  associated  with  it  which  involve  the  growth  of  great 
quantities  of  morbid  fibrous  tissue  in  the  thoracic  and  abdominal 
organs,  the  same  fibrous  growth  is  found,  if  sought,  in  the  spinal  cord. 
This  is  true  of  cases  in  which  there  were  not  at  any  time  symptoms 
pointing  to  disease  of  the  nervous  system.  Fig.  127  represents  the 
lumbar  cord  of  a  man  fifty-seven  years  old  who  died  of  Bright's  dis- 
ease, with  great  fibrosis  of  the  organs  and  extensive  calcareous  de- 
posits in  many  organs  and  tissues  and  in  the  arteries,  and  without 


FIG.  127. — PERIPHERAL  FIBROSIS  AND  ENLARGED  SOLID  CENTRAL  CANAL  OF  THE 
SPINAL  CORD.     (X  10.) 

Lumbar  cord  from  a  man  fifty-seven  years  old  who  died  of  Bright' s  disease.  Around 
the  periphery  throughout  almost  the  entire  circuit  the  tissue  is  condensed  and  fibrous. 
The  growth  has  been  from  without  inward,  and  in  the  thickened  portion  the  nerve  ele- 
ments have  disappeared.  At  e  the  thickening  reaches  its  maximum.  The  membranes 
are  more  closely  adherent  to  the  cord  than  is  natural.  The  central  canal  (h]  is  much 
enlarged,  is  solid,  and  no  epithelial  cells  can  be  seen  in  it.  Figs.  128  and  129  are  from 
the  same  case. 


Fie.  127. 


THE   SPINAL   CORD.  157 

nervous  symptoms.  The  drawing  represents  the  commonest  disease 
found  under  the  circumstances.  The  lesions  are  not  so  obvious  but 
that  they  might  escape  detection  unless  carefully  sought.  The  mem- 
branes are  more  closely  adherent  than  is  natural  around  the  entire 
cord,  and  the  nervous  tissue  adjacent  is  condensed  and  fibrous.  In 
these  areas  all  trace  of  nerve  elements  has  disappeared.  The  illustra- 
tion exhibits  a  very  slight  degree  of  the  change,  and  greater  amplifi- 
cation is  necessary  to  demonstrate  minutiae,  but  of  the  existence  of  the 
two  features  mentioned  there  can  be  no  doubt.  The  central  canal  is 
larger  than  natural,  is  quite  solid,  and  is  composed  of  cells  of  very 
peculiar  appearance,  there  being  no  trace  of  the  columnar  epithelium 
which  forms  so  characteristic  a  feature  of  the  central  canal  of  the  cord 
under  natural  conditions.  The  details  of  this  disease  of  the  central 
canal  will  be  more  fully  discussed  in  connection  with  Figs.  136  and 
137.  So  far  as  concerns  the  unnatural  adhesion  of  the  pia  mater  and 
thickening  and  fibrosis  of  the  adjacent  nervous  tissue,  the  parallel  is 
complete  between  such  disease  of  the  spinal  cord  and  the  fibrosis  of 
the  capsules  and  subjacent  parts  in  the  thoracic  and  abdominal  viscera 
which  has  been  said  to  be  of  such  frequent  occurrence.  In  this  con- 
nection it  may  be  mentioned  once  more  that  disease  very  commonly 
begins  in  the  envelopes  and  at  the  surface  of  the  organs.  The  cause 
for  this,  although  at  present  hidden  from  us,  should  be  diligently 
sought  after,  and  will  probably  some  day  be  found.  It  is  likely  that 
there  is  some  connection  between  this  special  vulnerability  to  disease 
on  the  part  of  the  surfaces  of  organs  and  their  envelopes  and  the  ar- 
terio-capillary  fibrosis  of  Gull  and  Sutton.  Although  in  their  studies 
they  confined  themselves  principally  to  the  blood-vessels,  they  at  the 
same  time  observed  certain  changes  in  the  spinal  cord  which  they 
minutely  describe  and  illustrate.*  There  is  every  reason  to  think 
that  they  were  to  some  extent  incorrect  in  their  conclusions  regarding 
the  condition  of  the  fibrous  coat  of  arterioles,  and  this  probably  was 
because  the  microscopical  technique  of  that  day  had  not  been  suffi- 
ciently perfected  to  enable  them  to  study  satisfactorily  the  finer  his- 
tological  conditions.  On  the  other  hand,  to  them  is  due  the  credit 
of  having  first  demonstrated  that  Bright's  disease  is  not  a  mere  kid- 
ney disease,  but  that  the  growth  of  morbid  fibrous  tissue  antedates 
the  kidney  lesions  and  is  of  greater  importance,  and  that  there  are 
morbid  lesions  widely  diffused  through  the  body. 

Fig.  128  is  a  section  of  the  cervical  cord  from  the  same  case  as  the 

*  Transactions  of  the  Royal  Medical  and  Chirurgical  Society. 


158  THE   ORIGIN   OF   DISEASE. 

preceding.  There  is  a  large  cyst  with  fibrous  walls  which  lies  in  such 
a  position  as  almost  entirely  to  cut  off  the  commissure.  Fig.  129  is 
another  picture  of  the  cervical  cord  from  the  same  case,  and  the  section 
was  cut  less  than  an  eighth  of  an  inch  away  from  the  one  represented 
by  Fig.  128.  In  Fig.  129  also  the  cyst  is  included,  but  instead  of  in- 
terrupting the  commissure  it  lies  entirely  behind  it,  in  the  white  sub- 
stance of  the  posterior  columns,  and  its  cavity  is  smaller  and  its  walls 
are  formed  of  much  thicker  fibrous  tissue,  from  which  strong  prolon- 
gations extend  in  various  directions  into  the  nervous  tissue  around 
it.  This  cyst  might  by  many  be  named  a  syringomyelia,  but,  what- 
ever syringomyelias  may  be,  and  however  they  are  caused,  the  cavity 
here  shown  presents  in  all  respects  the  characteristics  of  cysts  as  they 
appear  in  other  organs,  and  in  this  case  there  was  also  cystic  disease  of 
the  kidneys.  There  is  no  reason  to  suppose  that  the  cavity  is  any- 
thing but  a  cyst,  and  there  is  no  known  reason  why  cysts  should  not 
form  in  the  spinal  cord  as  well  as  in  the  substance  of  any  of  the  other 
organs.  Cysts  are  the  result  of  a  combination  of  morbid  fibroid 
growth  and  degeneration  of  tissue,  the  existence  of  the  two  processes 
together  appearing  to  be  essential  to  their  production.  A  cyst  of 
such  size  as  the  one  under  consideration  necessarily  caused  great 
destruction,  and  must  have  cut  off  a  great  many  nerve  fibres.  It  has 
been  very  generally  accepted  as  a  fact  that  such  a  destruction  of  nerve 
fibres  causes  degeneration  of  the  cord  for  a  considerable  distance  above 
and  below  the  region  destroyed.  These  secondary  degenerations  obey 
laws  which  are  thought  to  be  pretty  well  known,  and  they  extend 
upward  and  downward  in  the  cord  along  paths  which  have  been  de- 
termined by  the  observation  of  numerous  cases  of  localized  disease. 
In  a  paper  already  quoted  *  I  have  tried  to  show  that  this  conclusion 
goes  further  than  is  warranted  by  the  facts,  and  is  not  so  accurate  as 
is  generally  believed.  Study  of  the  cord  in  which  the  cyst  was  found 
confirms  the  views  previously  expressed,  and  perhaps  does  even  more, 
for  there  is  no  secondary  degeneration  below  the  area  of  destruction 
by  the  cyst.  Sections  both  of  the  dorsal  and  of  the  lumbar  cord, 
prepared  with  great  care  and  by  more  than  one  method,  failed  to  show 
the  slightest  sign  of  any  downward  degeneration.  Whether  there 
was  secondary  degeneration  extending  upward  in  the  cord  from  the 
cyst  cannot  be  known,  for  none  of  the  cord  above  the  cervical  portion 
which  contained  the  cyst  was  retained  for  examination.  This,  how- 
ever, makes  no  great  difference,  for,  although  it  would  have  made  the 

*  Page  155,  supra. 


FIG.  128. — CYSTIC  DISEASE  OF  THE  SPINAL  CORD.     (X  10.) 

Cervical  cord  from  the  same  case  as  Fig.  127.  The  cyst  lies  centrally  in  the  cord.  It 
is  larger  than  in  Fig.  129,  has  less  thick  fibrous  walls,  and  occupies  a  different  position,  so 
that  it  almost  entirely  cuts  off  the  commissure.  The  picture  makes  the  cord  appear  a  little 
smaller  than  Fig.  129  and  ol  lighter  color.  This  is  owing  to  a  different  mode  of  prepara- 
tion, which  caused  more  shrinking  of  the  tissue. 

FIG.  129. — CYSTIC  DISEASE,  FIBROSIS,  AND  DEGENERATION  OF  THE  SPINAL  CORD. 

(X  10.) 

Cervical  cord  from  the  same  case  as  Fig.  128.  The  section  here  represented  and  that 
shown  in  Fig.  128  were  not  more  than  an  eighth  of  an  inch  apart.  The  cyst  lies  in  the 
white  substance  behind  the  commissure.  Its  cavity  contained  liquid  and  some  solid 
structureless  material ;  the  enclosing  walls  are  of  dense  fibrous  tissue,  and  there  are  fibrous 
strands  extending  into  the  surrounding  nervous  tissue.  The  cyst  would  by  many  be  de- 
scribed as  a  syringomyelia.  a  is  a  region  in  which  the  fibrous  trabeculse  extending  inward 
from  the  periphery  and  the  fibrous  elements  generally  are  increased.  It  is  shown  more 
highly  magnified  by  Fig.  132.  b,  an  area  of  degeneration  ;  better  seen  in  Fig.  133,  which 
is  the  same  region  more  highly  magnified. 


FIG.  129. 


THE   SPINAL   CORD.  159 

observation  more  complete  to  have  found  upward  secondary  degen- 
eration absent,  the  proof  is  absolute  that  secondary  degenerations  up- 
ward and  downward  do  not  always  follow  as  a  consequence  of  local 
destructions,  since  it  has  been  shown  in  a  single  case  that  there  was 
no  downward  degeneration  caused  by  such  extensive  local  destruction 
as  that  occasioned  by  the  cyst  which  has  been  described.  The  por- 
tion of  cord  illustrated  by  Fig.  129  shows  other  evidence  of  fibroid 
disease  besides  the  curious  and  interesting  lesions  already  described. 
It  should  be  kept  constantly  in  mind  that  the  case  was  one  of  Bright's 
disease  in  which  the  kidneys  were  cystic  and  there  was  an  extraordi- 
nary increase  of  fibrous  tissue  through  the  body,  in  the  organs,  and 
in  the  blood-vessels,  with  calcareous  deposits  to  an  unusual  extent. 
In  Fig.  129  it  can  be  seen  that  the  fibrous  prolongations  from  the 
pia  mater  covering  the  surface  of  the  cord  are  strong  and  heavy  and 
extend  as  black  lines  deeply  into  the  nervous  tissue.  It  is  a  well- 
established  anatomical  fact  that  these  extensions  from  the  pia  mater 
are  natural,  and  that  they  constitute  the  fibrous  framework  which  sup- 
ports the  delicate  nerve  tissue,  and  contain  the  blood-vessels  which 
supply  nutriment.  The  trabeculae,  however,  in  this  cord  are  much 
thicker  than  is  natural.  In  sharp  contrast  with  the  increase  of 
density  at  the  periphery,  which  is  owing  partly  at  least  to  the  growth 
of  morbid  fibrous  tissue,  are  the  open  structure  and  torn  appearance 
of  the  central  portion  near  the  gray  matter,  especially  in  one  of  the 
antero-lateral  columns.  These  two  conditions,  the  dense  and  fibrous 
state  at  the  periphery  and  the  open  nature  of  the  tissue  near  the  gray 
matter,  are  well  shown  so  far  as  concerns  their  situation  and  general 
effects  by  Fig.  129,  but  to  obtain  an  accurate  comprehension  of  the 
changes  which  have  been  produced  by  the  disease  it  is  necessary  to 
examine  Figs.  132  and  133,  which  are  more  highly  magnified  views 
of  portions  of  tissue  representative  of  the  two  regions.  Fig.  132, 
which  is  from  the  periphery,  shows  nerve  fibres  which  are  natural 
except  that  in  a  few  of  them  there  are  slight  indications  of  an  early 
stage  of  degeneration ;  but  the  condition  of  the  fibrous  tissue  is  very 
different :  the  trabeculae,  two  of  which  are  included,  are  very  much 
thickened  and  dense  in  structure.  Even  the  fine  fibrous  strands  that 
ramify  among  the  individual  nerve  fibres  have  been  tainted  by  the 
general  fibroid  growth  and  are  less  delicate  than  natural.  Fig.  133, 
which  represents  a  portion  of  the  cord  near  the  gray  horn,  is  seen  at 
a  glance  to  present  the  greatest  difference  from  the  last-described  pic- 
ture. Instead  of  the  nerve  fibres  filling  almost  the  entire  space,  each 


160  THE   ORIGIN   OF   DISEASE. 

being  a  discrete  whole,  composed  of  an  axis  cylinder,  white  substance 
of  Schwann,  and  encircling  envelope,  and  closely  surrounded  by  other 
similar  nerves,  the  general  effect  is  rather  of  confusion  than  of  a  well- 
ordered  arrangement.  There  are  scattered  and  broken  shreds  of 
fibrous  tissue  which  form  spaces  of  very  various  shapes  and  sizes. 
Some  of  these  spaces  appear  empty,  or  there  are  axis  cylinders  which 
have  not  around  them  the  natural  cylinder  of  white  substance  and  en- 
circling envelope.  Again,  there  are  nerve  fibres  which  appear  natural 
except  that  their  white  substance  of  Schwann  is  muddy.  The  torn 
appearance  of  the  tissue  is  striking,  but  besides  this  there  is  a  de- 
cided increase  of  the  amount  of  fibrous  tissue,  the  strands  being  wider 
than  natural,  although  less  dense  in  structure  than  the  trabeculae  in 
Fig.  132.  The  tearing  apart  must  have  been  effected  by  some  effusion 
such  as  occurs  in  the  subcutaneous  tissues  in  anasarca. 

In  considering  the  illustrations  of  spinal  cord  which  have  been  thus 
far  described,  it  must  be  remembered  that  all  of  them  are  from  the 
same  case,  a  man  fifty-seven  years  old  who  died  of  Bright's  disease 
but  without  having  had  any  clinical  symptoms  to  indicate  disease 
of  the  nervous  system.  The  lesions  found  were  briefly  as  follows  : 
adhesion  of  the  pia  with  slight  fibrosis  of  the  adjacent  nervous  tissue, 
and  a  large  cyst  which  had  not  caused  any  secondary  downward  de- 
generation, thus  disproving  the  accepted  doctrine  that  destructions  of 
the  cord  always  produce  secondary  degeneration  above  and  below  the 
primary  lesion.  Further,  there  was  fibrosis  of  the  peripheral  region, 
the  nerves  remaining  almost  natural,  while  near  the  centre  of  the  cord, 
besides  the  fibrosis,  which  was  of  different  character  from  that  at  the 
periphery,  the  nerves  were  degenerated  and  the  tissue  torn  by  the 
action  of  some  material  which  had  been  effused  into  it.  The  discovery 
of  so  many  lesions  of  the  nerves  in  a  case  from  which  all  symptoms 
of  nervous  disease  had  been  absent  is  very  instructive  when  taken  in 
connection  with  what  has  been  so  frequently  said,  that  lesions  may 
often  be  found  if  sought  in  organs  in  which  there  was  no  reason  to 
suspect  their  existence  from  anything  in  the  life-history  of  the  patient. 

Figs.  1 30  and  131  are  from  a  man  forty-two  years  of  age  who  died 
of  organic  heart  disease,  a  different  condition  therefore  from  the  pre- 
ceding case,  but  at  the  same  time  one  closely  allied  to  it,  for  the  fact 
is  well  established  that  Bright's  disease  and  chronic  heart  disease  are 
intimately  connected.  The  attempt  has  often  been  made  to  learn 
what  the  relation  between  the  two  diseases  is,  but  nothing  conclusive 
has  been  discovered ;  however,  the  establishment  of  the  fact  that  there 


FIG.  130. — DEGENERATION  OF  THE  SPINAL  CORD  IN  HEART  DISEASE,     (x  400.) 

Section  of  the  dorsal  cord  of  a  man  of  forty-two  years  who  died  of  organic  heart 
disease.  The  drawing  is  of  a  portion  of  the  periphery,  and  includes  pia  mater  (p]  and 
adjacent  tissue.  All  sharpness  of  outline  has  been  destroyed.  Only  a  few  of  the  nerve 
fibres  have  distinct  axis  cylinders  and  clean  white  substance  of  Schwann  ;  in  most,  the 
white  substance  has  become  muddy,  the  axis  cylinders  are  ill  defined,  and  the  whole  of 
the  tissue  is  melting  into  a  structureless  granular  mass. 

FIG.  131. — DEGENERATION  OF  A  PERIPHERAL  NERVE  IN  HEART  DISEASE,     (x  400.) 

From  the  same  section  as  Fig.  130,  a  portion  of  one  of  the  peripheral  nerves,  n  is  a 
large  nerve  fibre  from  which  the  axis  cylinder  has  entirely  disappeared  and  in  which  the 
white  substance  of  Schwann  is  becoming  muddy  and  granular.  Many  of  the  others  are 
in  a  similar  condition  of  destruction.  In  some  fibres  the  white  substance  is  even  more 
granular  than  in  n  and  the  axis  cylinders  are  gone,  or  again  the  white  substance  is  very 
muddy  but  the  axis  cylinders  remain,  /"denotes  small  nerve  fibres  which  are  very  diseased. 
The  small  fibres  in  a  natural  condition  are  as  distinct  as  the  large  ones,  but  nearly  all  those 
included  in  the  drawing  are  so  disintegrated  that  they  appear  as  masses  of  densely  gran- 
ular material  containing  ill-defined  circles.  The  extreme  development  of  this  disease  is 
the  conversion  of  nerve  fibres  into  morbid  fibrous  tissue,  as  seen  at  such  places  as  l>,  b. 
h  indicates  two  small  nerve  fibres  which  still  preserve  all  their  distinctive  characters  but 
are  in  the  first  stage  of  degeneration,  for  their  white  substance  of  Schwann  is  muddy. 
The  degeneration  shown  by  the  drawing  is  an  advanced  stage. 

FlG.    132. — FlBROSIS   OF   THE  SPINAL   CORD    IN    BRIGHT'S    DISEASE.       (X  4OO.) 

The  region  a  of  Fig.  129,  more  highly  magnified.  It  is  from  the  antero-lateral 
column  at  the  periphery.  /,  pia  mater,  and  /,  /,  fibrous  trabeculse  extending  from  it  in- 
ward. These  fibrous  columns  and  the  pia  are  thick  and  heavy.  The  nerve  substance 
itself  is  fairly  healthy,  the  nerve  fibres  and  axis  cylinders  being  sharply  outlined  and  the 
white  substance  of  Schwann  generally  clean  and  white.  In  a  few  of  the  nerves  the  white 
substance  is  a  little  muddy.  There  is  probably  slight  increase  of  the  delicate  fibrous 
strands  among  the  individual  nerve  fibres.  The  nerves  present  a  strong  contrast  with 
those  of  Fig.  133,  which  are  greatly  altered  by  disease. 

FIG.  133. — DISINTEGRATION  OF  THE  SPINAL  CORD  IN  BRIGHT'S  DISEASE,     (x  400.) 

The  region  b  of  Fig.  129,  more  highly  magnified.  A  part  of  the  antero-lateral  column 
near  the  gray  horn.  The  fibrous  tissue  is  increased,  but  is  of  much  less  dense  structure 
than  that  of  Fig.  132.  The  outlines  of  the  nerve  fibres  are  ill  defined,  one  not  being 
sharply  separated  from  another.  In  places  the  axis  cylinders  have  disappeared  and  left 
large  irregularly  divided  spaces  which  appear  empty.  The  white  substance  of  Schwann 
of  many  nerve  fibres  is  muddy  instead  of  pure  white.  The  difference  of  the  torn  fibrous 
tissue  of  this  region  from  the  thickened  and  dense  columns  of  Fig.  132  is  very  great. 


Fig.131 


Fig.  130 


THE   SPINAL   CORD.  161 

is  a  connection  makes  me  believe  there  must  be  a  common  underlying 
cause  which  induces  both  of  them.  Fig.  130  exhibits  a  condition  of 
disease  which  could  not  have  been  of  very  long  standing,  for  the  de- 
struction of  nerve  fibres  is  so  complete  and  extends  over  so  great  a 
surface  that  a  considerable  portion  of  the  cord  must  have  been  ren- 
dered useless.  There  are  hardly  any  nerve  fibres  which  have  distinct 
axis  cylinders  and  clean  white  substance  of  Schwann.  In  most  of 
them  the  white  substance  is  muddy,  the  axis  cylinders  are  ill  defined, 
the  external  envelopes  are  indistinct  or  lost,  and  the  whole  of  the  tis- 
sue is  melting  into  a  structureless  granular  mass.  A  lesion  like  this 
was  almost  certainly  developed  during  the  latter  part  of  the  final  ill- 
ness, with  the  universal  disturbance  of  the  circulation  and  of  the 
organs  which  occurs  toward  the  end  in  persons  dying  of  organic  heart 
disease.  Besides  the  disease  which  has  been  described,  there  were 
thickening  of  the  pia,  adhesion  to  the  cord,  and  increase  of  the  fibrous 
elements.  Fig.  131  is  a  portion  of  a  peripheral  nerve  which  lay  within 
the  spinal  canal,  and  it  was  included  in  the  same  section  with  Fig  130. 
The  disease  is  as  different  as  possible  from  that  shown  by  Fig.  130, 
and  must  have  been  of  much  longer  standing.  There  are  chronic 
fibrosis  and  degeneration  of  the  nerves.  The  larger  nerves  show  a 
variety  of  changes  due  to  disease,  and  hardly  any  of  them  can  be 
said  to  be  entirely  natural.  From  many  the  axis  cylinders  have 
disappeared,  and  in  such  the  white  substance  is  muddy  and  of  a 
yellowish  color  quite  different  from  that  of  healthy  fibres.  In  others 
the  axis  cylinders  are  enlarged,  or  their  outlines  are  ill  defined,  or 
they  have  lost  their  solid  look  and  appear  as  empty  rings.  The 
small  fibres  are  perhaps  even  more  greatly  changed  than  the  large 
ones.  In  healthy  tissue  the  small  nerve  fibres  are  exactly  like  the 
large  ones  except  in  size,  being  composed  of  a  distinct  axis  cylinder, 
white  substance  of  Schwann,  and  sharply  defined  external  enveloping 
ring.  No  such  fibres  are  to  be  seen  in  the  picture.  There  are  a  few  in 
which  the  three  component  parts  can  all  be  distinguished,  but  even  in 
these  the  white  substance  is  muddy.  Most  of  the  small  fibres  have 
lost  their  distinctive  characters  and  appear  as  confused  masses  of  gran- 
ular tissue  containing  rings,  which  are  the  remains  of  the  external  en- 
velopes of  the  fibres.  Various  stages  of  this  degeneration  are  to  be 
seen,  and  it  is  evident  that  the  process  is  one  of  fibrosis  in  which  the 
nerve  fibres  themselves  to  a  considerable  extent  are  converted  into 
morbid  fibrous  tissue.  The  nature  of  the  lesions  shown  by  this  picture 
— fibrosis  and  this  form  of  nerve  degeneration — is  such  that  it  is  cer- 

ii 


162  THE   ORIGIN   OF   DISEASE. 

tain  they  had  existed  for  a  considerable  time  before  death,  and  yet,  as 
in  the  first-mentioned  case,  there  had  been  no  symptoms  of  disease 
of  the  nervous  system. 

In  the  case  which  furnished  the  illustrations  next  to  be  described, 
a  very  different  state  of  affairs  obtained.  The  patient  died  at  seventy 
years  of  age,  having  had  for  about  ten  years  the  symptoms  of  chronic 
degeneration  of  the  spinal  cord.  His  muscular  power  gradually  di- 
minished until  he  could  neither  walk  nor  stand  alone,  although  there 
was  no  actual  paralysis  of  any  part.  The  muscles  seemed  stiff  and 
hard,  and  when  any  movement  was  made  it  took  him  a  long  time  to 
begin,  and  then  it  was  executed  very  slowly.  This  delay  to  begin  and 
slowness  to  execute  movements  after  it  has  become  evident  that  the 
person  intends  to  perform  some  act  requiring  the  use  of  the  muscles 
are  characteristic  features  of  spinal  degeneration,  such  as  this  man 
had.  At  the  same  time  he  grew  very  fat  and  his  mind  degenerated. 
There  was  no  insanity,  but  he  became  irritable,  his  memory  was 
impaired,  and  he  was  incompetent  for  any  mental  effort.  During  the 
course  of  the  progressively  increasing  feebleness  there  was  nothing 
to  indicate  other  disease  than  that  of  the  nervous  system,  except  that 
the  very  first  sign  of  a  departure  from  perfect  health  was  an  attack  of 
acute  catarrhal  pneumonia  about  ten  years  before  he  died.  There 
never  was  any  clinical  evidence  of  disease  of  the  kidneys,  no  albumen 
nor  casts  in  the  urine,  nor  any  abnormal  lowering  of  the  specific 
gravity,  and  yet  after  death  there  was  found  fibrosis  of  the  heart, 
lungs,  liver,  and  spleen,  and  the  kidneys  were  greatly  contracted  and 
their  blood-vessels  showed  a  great  variety  of  disease.  Fig.  134,  which 
represents  a  section  of  the  lumbar  cord  from  the  case  of  chronic  myeli- 
tis just  described,  exhibits  important  lesions.  The  tissue,  especially 
toward  the  periphery,  is  torn  apart,  so  that  it  presents  as  open  an 
appearance  as  a  sieve,  instead  of  being  evenly  solid  as  natural  spinal 
cord  is,  and  the  central  canal  is  enlarged  and  solid.  The  torn  con- 
dition may  be  positively  asserted  to  be  the  result  of  effusion  into  the 
tissue  of  the  nature  of  dropsy.  Of  course  the  first  thought  that  enters 
the  mind  of  a  pathologist  upon  seeing  so  singular  an  appearance  as 
that  represented  by  the  drawing  is  that  the  effect  was  produced  after 
death,  owing  to  some  fault  in  the  preservation  or  mounting  of  the 
tissue  for  examination  with  the  microscope,  and  that  it  is  not  disease, 
but  post-mortem  change.  This  was  my  own  conclusion  when  spinal 
cord  thus  torn  apart  first  came  to  my  notice.  The  condition,  which  I 
have  called  dropsy  of  the  spinal  cord,  is  not  rare  in  persons  dead  of 


FIG.  134. — DROPSY,  UNIVERSAL  DEGENERATION,  AND  ENLARGED  SOLID  CENTRAL 
CANAL  OF  THE  SPINAL  CORD,     (x  10.) 

Section  of  the  dorsal  cord  from  a  man  seventy  years  old  who  died  of  chronic  myelitis. 
The  whole  of  the  peripheral  portion  is  torn  and  shredded  out,  while  toward  the  centre  it 
is  less  diseased,  g  is  the  central  canal,  which  is  much  enlarged  and  quite  solid.  Figs. 
136  and  137  are  enlarged  views  of  this  central  canal.  Fig.  135  depicts  more  highly 
magnified  a  portion  from  the  periphery  and  another  portion  near  the  centre  of  this  same 
cord,  h  indicates  a  region  where  the  tissue  was  slightly  torn  in  preparation. 

FIG.  135. — DEGENERATION  OF  THE  WHITE  SUBSTANCE  OF  THE  SPINAL  CORD,    (x  220.) 

From  the  same  cord  as  Fig.  134,  but  another  section  differently  stained.  More  highly 
magnified  view.  a,  from  periphery  ;  b,  from  central  portion.  In  a  the  tissue  is  torn 
apart  and  no  nerve  fibres  of  large  size  remain  ;  while  in  the  fibres  still  present  the  axis 
cylinders  are  enlarged  and  not  sharply  defined  from  the  surrounding  white  substance  of 
Schwann,  which  is  muddy.  There  is  fibrous  increase,  and  an  amylaceous  body  is  included. 
b,  from  the  central  portion,  is  less  diseased.  The  axis  cylinders  of  the  large  nerves  are 
small,  ill  outlined,  and  some  of  them  eccentrically  placed.  The  smaller  fibres  are  not 
sharply  outlined,  and  the  white  substance  of  Schwann  is  muddy.  Many  nerve  fibres  have 
disappeared,  and  are  replaced  by  the  dark  material,  which  is  morbid  fibrous  tissue.  The 
most  striking  contrast,  perhaps,  is  that  a  is  broken  and  has  torn  and  scattered  shreds  of 
nerves,  while  b  is  a  solid  tissue. 


FIG.  135. 


THE   SPINAL   CORD.  163 

chronic  disease,  even  if  there  were  no  clinical  symptoms  of  nervous 
disease  during  life.  For  some  time  after  first  seeing  the  lesion  I  sup- 
posed it  was  caused  by  fault  in  my  technique,  but  at  last  I  was  shaken 
in  this  opinion  by  finding  in  one  of  my  cases  that,  although  different 
pieces  of  the  tissue  were  prepared  and  mounted  in  various  ways,  the 
appearance  of  the  dropsy  was  equally  distinct  in  all  of  them.  After 
having  found  this  sufficiently  often  it  was  impossible  to  continue  to 
believe  it  a  post-mortem  change  or  due  to  bad  technique,  and  I  was 
driven  to  the  conclusion  that  it  must  be  a  state  of  disease.  There  is 
no  reason  why  effusion  producing  a  condition  of  dropsy  should  not 
occur  as  well  in  the  spinal  cord  as  elsewhere,  especially  as  the  cases 
in  which  the  lesion  is  most  frequently  found  are  those  chronic  ones  in 
which  transudation  into  the  cavities,  tissues,  and  organs  is  common. 
In  the  case  under  consideration  four  sets  of  sections  of  the  cord  were 
prepared  separately,  two  by  a  skilled  microscopist  and  two  by  myself, 
and  in  all  of  them  the  cord-tissue  had  the  same  sieve-like  appearance. 
Consideration  of  the  reasons  that  have  been  detailed  warrants  the  con- 
clusion that  the  lesion  is  the  result  of  transudation  and  constitutes  a 
true  dropsy  of  the  spinal  cord. 

In  addition  to  the  dropsy,  which  is  so  well  shown  by  the  drawing, 
the  tissue  is  degenerated,  but  this  can  hardly  be  distinguished  without 
greater  amplification.  Fig.  135  represents,  more  highly  magnified, 
two  portions  of  the  tissue  shown  in  Fig.  134,  one  from  the  periphery 
and  the  other  from  the  centre  near  the  gray  horn.  The  drawing  of 
the  peripheral  region  (a)  makes  very  evident  the  dropsy ;  the  tissue  is 
so  torn  apart  as  to  give  the  impression  of  a  great  amount  of  empty 
space,  the  amount  of  this  apparently  empty  space  which  was  filled  by 
the  transuded  material  exceeding  that  occupied  by  solid  tissue.  The 
solid  tissue  is  all  greatly  degenerated.  The  axis  cylinders  are  enlarged 
and  their  outlines  are  not  sharply  defined  from  the  surrounding  white 
substance  of  Schwann,  which  is  muddy  instead  of  being  entirely  un- 
stained as  is  the  case  in  healthy  fibres.  Morbid  fibrous  tissue  lies 
among  the  fibres,  having  grown  at  the  expense  of  the  nerves,  and  one 
of  the  bodies  which  have  been  named  corpora  amylacea  is  included. 
They  are  produced  only  by  degeneration.  Such  an  effect  must  have 
been  produced  in  the  course  of  a  long  period  by  the  gradual  growth 
of  fibrous  tissue  and  degeneration  of  the  nervous  elements,  and,  finally, 
not  long  before  death  came  the  dropsical  transudation  which  tore 
open  the  tissue  and  completed  the  work  of  destruction. 

The  tissue  from  the  centre  near  the  gray  matter  (b,  Fig.  135)  pre- 


164  THE   ORIGIN   OF   DISEASE. 

sents  the  strongest  contrast  to  that  from  the  periphery.  It  is  quite 
solid  and  firmly  knit,  and  yet  shows  evidence  of  disease  as  unmis- 
takable as  the  torn  tissue.  The  most  striking  and  certainly  the  most 
important  feature  is  the  increase  of  fibrous  tissue.  The  strands  run- 
ning among  the  nerve  fibres  are  heavy,  but  still  more  striking  is  the 
conversion  of  the  smaller  nerves  into  morbid  fibrous  tissue.  None  of 
the  small  fibres  are  natural  in  appearance.  They  are  dark-colored, 
and  the  outlines  of  their  component  parts  are  indistinct.  In  none  of 
them  is  the  white  substance  unstained  and  white  as  in  healthy  nerves, 
and  the  axis  cylinders  and  "external  envelopes  of  the  fibres  are  in  all 
stages  of  indistinctness.  In  natural  cord  almost  all  the  space  between 
the  large  fibres  is  filled  by  small  ones  whose  characteristics  are  as  dis- 
tinct as  those  of  larger  size.  In  the  picture  the  space  between  the 
large  fibres  is  occupied  by  morbid  fibrous  tissue  which  was  formed  out 
of  destroyed  nerve  fibres  and  by  other  fibres  which  are  in  all  stages 
of  degeneration,  and  which  were  evidently  in  process  of  destruction 
and  would  have  been  converted  into  fibrous  tissue  had  life  been  suf- 
ficiently prolonged.  The  large  fibres  also  are  diseased,  although  much 
less  so  than  the  small  ones.  Their  axis  cylinders  are  eccentrically 
placed,  are  rather  small,  and  have  not  the  sharpness  of  outline  of 
healthy  nerve  fibres.  No  part  of  the  tissue,  therefore,  was  in  a  natural 
condition. 

It  was  mentioned  in  connection  with  Fig.  1 34  that  the  central  canal 
of  the  cord  is  enlarged  and  solid,  but  the  structure  and  peculiarities 
were  not  described.  Fig.  136  is  this  central  canal  more  magnified,  and 
it  shows  a  curious  condition  of  disease.  It  is  well  known  that  the  cen- 
tral canal  changes  as  life  advances,  and  the  following  expresses  the 
accepted  views  of  histologists  upon  the  subject :  "  The  cords  of  chil- 
dren and  of  many  animals  contain  a  completely  pervious  central  canal ; 
in  the  human  cord  in  later  life  this  is  usually  more  or  less  occluded, 
although  much  variation  exists  in  this  respect.  The  upper  cervical, 
lower  lumbar,  and  sacral  regions  usually  contain,  even  in  the  adult,  a 
partially  pervious  tube.  Overgrowth  of  the  lining  cells,  as  well  as  the 
subepithelial  substantia  gelatinosa,  is  the  principal  factor  in  the  closure 
of  the  central  canal,  which,  however,  must  be  regarded  as  a  normal 
change  and  not  a  pathological  process."  *  The  changes  which  take 
place  in  the  tissues  between  birth  and  old  age  are  highly  interesting, 
and  it  is  quite  true  within  certain  limits  to  say  that  those  described  as 
occurring  in  the  central  canal  must  be  regarded  as  normal  and  not  as 

*  Normal  Histology,  by  George  A.  Piersol,  Philadelphia,  1893. 


FIG.  136. — ENLARGED  SOLID  CENTRAL  CANAL  CONTAINING  A  BLOOD-VESSEL,    (x  50.) 

Section  of  the  lumbar  cord  from  the  same  case  as  Fig.  134.  a  denotes  the  anterior 
and  b  the  posterior  aspect,  c  and  d  are  the  two  lateral  boundaries  of  the  central  canal, 
which  is  very  large,  completely  solid,  and  shows  no  trace  of  epithelial  cells.  Its  anterior 
and  posterior  boundaries  are  easy  to  distinguish  in  the  drawing,  e  is  a  blood-vessel.  Fig. 
137  is  an  enlarged  view  of  the  blood-vessel  (e)  and  surrounding  material. 

FIG.  137. — BLOOD-VESSEL  IN  THE  ENLARGED  SOLID  CENTRAL  CANAL  OF  THE  SPINAL 

CORD,     (x  220.) 

Enlarged  view  of  the  vessel  e  in  Fig.  136  and  of  the  surrounding  cells.  The  vessel 
contains  many  red  and  white  blood-corpuscles  and  in  structure  is  like  a  capillary.  The 
cells  by  which  it  is  surrounded  are  of  unusual  appearance  and  cannot  be  satisfactorily 
classified.  They  are  not  epithelial,  nor  are  they  like  leucocytes.  It  is  evident  that  the 
material  which  filled  the  central  canal  and  enlarged  and  made  it  solid  was  a  living  growing 
tissue  with  a  blood-supply,  but  its  cellular  composition  is  not  like  that  of  any  of  the  ordi- 
nary tissues. 


FIG.  136. 
a 


e          d 


FIG.  137. 


THE   SPINAL   CORD.  165 

pathological  processes.  On  the  other  hand,  it  is  equally  true  that  it  is 
very  common  for  such  changes  to  become  so  exaggerated  that  they 
must  be  looked  upon  as  pathological.  The  difficulty  of  the  question 
is  reached  when  the  attempt  is  made  to  decide  in  an  individual  case 
whether  conditions  found  are  to  be  classified  as  belonging  to  the 
normal  changes  or  are  pathological.  Fig.  136  exhibits  a  peculiarity 
which  settles  any  question  that  might  be  raised  as  to  whether  the 
tissue  is  diseased :  there  is  a  blood-vessel  in  the  very  centre  of  the 
solid  tissue  which  was  once  the  canal.  The  vessel  was  found  to 
be  present  in  a  number  of  sections  of  this  portion  of  the  cord.  No 
one  has  ever  pretended  to  say  that  blood-vessels  like  this  exist  in 
the  normal  central  canal  of  the  cord,  which  is  the  remnant  of  the 
neural  tube  of  the  embryological  period.  This  blood-vessel  is  in 
structure  like  the  normal  capillaries.  It  belongs  to  the  class  of 
vessels  which  are  prone  to  develop  in  new  tissues  or  in  tissues  which, 
owing  to  hypertrophy,  outgrow  their  ordinary  vascular  supply.  Be- 
sides the  positive  evidence  of  disease  afforded  by  the  presence  of  a 
blood-vessel  in  the  normally  avascular  central  canal,  the  nature  of  its 
tissue,  its  size,  and  its  relations  to  the  surrounding  nervous  tissue  are 
such  as  to  render  it  impossible  to  consider  it  a  normal  condition.  The 
description  quoted  shows  that  closure  of  the  canal  is  a  common  occur- 
rence. The  lining  cells  are  well  known  to  be  columnar  epithelium, 
and  in  the  young  human  subject  and  even  in  elderly  persons  their 
columnar  character  is  often  easy  to  recognize.  The  histological  de- 
scription is  that  the  cells  of  the  canal  undergo  proliferation  until  the 
central  space  is  closed,  but  it  is  not  asserted  that  it  ever  becomes 
greatly  enlarged  and  its  cellular  formation  entirely  changed.  In  the 
drawing  nothing  resembling  in  the  slightest  degree  the  natural  epi- 
thelium can  be  seen,  and  the  canal  is  at  least  two  or  three  times  larger 
than  natural.  Its  boundaries  are  shown  by  the  drawing,  and,  besides 
the  great  enlargement,  it  is  seen  to  have  grown  in  such  a  way  as  to 
imitate  the  appearances  produced  by  a  neoplastic  tumor  growing  in 
one  of  the  organs.  At  its  periphery  the  tissue  is  arranged  in  curving 
lines,  and  at  the  junction  of  the  diseased  tissue  with  the  surrounding 
nerve  substance  the  two  merge  together  in  such  a  way  that  it  is  hard 
to  say  exactly  where  one  ends  and  the  other  begins.  Some  such  effect 
is  always  produced  when  growth  takes  place  from  a  central  point  so 
rapidly  that  the  surrounding  parts  are  destroyed  or  squeezed  aside  to 
make  room  for  a  new  and  enlarging  tissue.  The  imitation  of  tumor 
growth  with  crushing  and  destruction  of  the  surrounding  nervous 


1 66  THE   ORIGIN   OF   DISEASE. 

material  could  hardly  be  more  striking  than  it  is,  and  it  is  impossible 
that  such  growth  should  have  occurred  without  injury  to  the  cord. 
Fig.  137  is  an  enlarged  view  of  the  blood-vessel  and  surrounding  tis- 
sue from  Fig.  136,  and  shows  that  it  is  structurally  like  a  capillary 
and  contains  both  red  and  white  corpuscles  and  is  surrounded  by  a 
lymph-space.  In  all  these  particulars  its  characteristics  are  the  same 
as  those  of  new  blood-vessels,  which  have  already  been  described  as 
they  develop  in  new  or  hypertrophied  tissues  (Chapter  IV.).  The  tis- 
sue by  which  the  vessel  is  surrounded  is  difficult  to  describe.  It  is  not 
like  epithelium,  connective  tissue,  or  any  of  the  normal  gland-cells,  but 
is  evidently  a  cellular  structure  of  aberrant  type,  and  therefore  should 
be  classed  with  the  tumor  growths.  Before  finally  leaving  the  con- 
sideration of  this  curious  case  of  chronic  myelitis,  which  proved  also 
to  be  one  of  Bright's  disease,  it  may  be  well  to  pass  in  review  the 
lesions  which  were  found  as  the  result  of  careful  microscopical  exami- 
nation of  sections  of  the  cervical,  dorsal,  and  lumbar  portions  of  the 
spinal  cord,  (i)  The  tissue  was  torn  apart  and  split  open  so  as  to 
present  an  almost  sieve-like  appearance;  this  has  been  said  to  be  a 
form  of  dropsy.  (2)  Near  the  periphery  there  was  extensive  fibrosis 
and  the  pia  mater  was  adherent  to  a  greater  degree  than  natural. 
(3)  The  central  canal  was  solid  and  enlarged,  the  columnar  epithelial 
cells  had  entirely  disappeared,  and  new  vessels  had  developed  in  the 
proliferated  tissue.  (4)  Throughout  the  cord  there  was  general  fibrosis, 
and  the  nerves  were  greatly  degenerated  and  many  of  them  destroyed. 
The  impression  was  that  the  actual  number  of  nerves  was  less  than  in 
healthy  nerve- tissue.  The  changes  were  most  extensive  in  the  pos- 
terior columns.  (5)  There  were  many  corpora  amylacea,  and  the 
Deiters  spider-cells  seemed  too  numerous  and  prominent.  (6)  The 
multipolar  ganglion-cells  gave  the  impression  of  being  less  numerous 
than  usual,  and  appeared  shrunken  and  ill  preserved.  (7)  The  periph- 
eral nerves  included  with  the  sections  of  the  cord  were  fibroid. 

Throughout  what  has  been  written  of  the  thoracic  and  abdominal 
organs  and  lastly  of  the  spinal  cord  the  fact  has  been  repeatedly 
dwelt  upon  that  pathological  lesions  are  often  found,  if  sought,  in 
other  organs  than  those  in  which  they  might,  from  the  life-history, 
have  been  expected,  such  lesions  having  occasioned  no  clinical  symp- 
toms to  direct  attention  to  organs  greatly  diseased.  Ordinarily  in 
cases  of  chronic  disease  many  of  the  viscera,  and  occasionally  all  of 
them,  are  involved.  To  a  certain  extent  the  lesions  found  in  different 
organs  are  similar,  although  the  clinical  manifestations  are  infinitely 


THE   SPINAL   CORD.  167 

various,  sometimes  one  and  sometimes  another  of  them  being  the 
victim  upon  which  the  disease  falls.  The  similarity  consists  in  this : 
no  matter  how  much  the  lesions  may  vary  in  other  respects,  increase 
of  fibrous  tissue  and  vascular  disease  are  common  to  them  all. 

All  the  illustrations  of  the  spinal  cord  which  have  been  described 
were  furnished  by  three  cases,  and  they  afford  an  interesting  con- 
firmation of  the  fact  that,  with  lesions  somewhat  parallel  and  of  wide- 
spread extent,  the  clinical  manifestations  were  as  different  as  it  was 
possible  for  them  to  be,  and  there  was  no  evidence  in  regard  to  how 
many  and  which  of  the  organs  were  diseased.  The  first  case  was  one 
of  Bright's  disease  with  extensive  organic  disease  of  the  thoracic  and 
abdominal  viscera,  but  no  symptoms  of  nervous  disease,  and  yet  the 
lesions  of  the  spinal  cord  were  of  so  gross  a  character  that  it  was  won- 
derful how  they  could  have  existed  without  external  manifestation  of 
their  presence.  The  second  case  was  one  of  disease  of  the  heart,  and 
was  like  the  first  in  the  relation  of  symptoms  to  lesions.  With  or- 
ganic disease  of  the  heart  and  of  other  organs  and  the  ordinary  clini- 
cal symptoms  manifest,  there  was  nothing  in  the  life-history  to  indi- 
cate involvement  of  the  nervous  system,  and  yet  the  lesions  of  the 
cord,  although  less  coarse,  were  as  unmistakable  as  those  found  in  the 
first  case.  In  the  third  case  the  conditions  were  exactly  reversed : 
from  the  beginning  it  was  evidently  one  of  disease  of  the  nervous  sys- 
tem, and  there  were  never  any  symptoms  indicating  involvement  of 
the  thoracic  and  abdominal  organs.  Although  disease  of  the  kidneys 
was  always  suspected,  no  evidence  of  its  existence  during  life  could 
at  any  time  be  obtained.  The  autopsy  demonstrated  that,  besides  the 
destructive  lesions  of  the  spinal  cord,  contracted  kidney  and  fibroid 
disease  of  other  organs  existed. 

No  three  cases  could  more  strikingly  demonstrate  the  existence  of 
lesions  in  other  organs  than  those  in  which  they  might  have  been  ex- 
pected from  a  routine  interpretation  of  the  clinical  symptoms.  The 
three  cases  illustrate  also  the  wide-spread  extent  of  organic  lesions  in 
chronic  disease.  Although  so  instructive  if  properly  appreciated,  the 
symptoms  and  disease  which  have  been  described  are  all  of  every-day 
occurrence. 

Besides  what  has  been  detailed  of  disease  of  the  spinal  cord,  many 
curious  things  have  come  to  my  attention  in  the  course  of  the  ex- 
amination of  cords  taken  from  cases  of  various  diseases.  In  typhoid 
fever,  for  instance,  the  cord  is  never  healthy.  The  appearances  are 
not  easy  to  describe,  and  are  perhaps  even  more  difficult  to  interpret, 


i68  THE   ORIGIN   OF   DISEASE. 

because  in  diseases  like  typhoid  fever,  in  which  the  blood  is  greatly 
disorganized,  the  tissues  are  always  in  a  condition  which  renders 
them  unsatisfactory  for  microscopical  examination.  The  cells  do  not 
differentiate  sharply,  and  all  the  tissues  are  clouded  and  obscure. 
It  is  not  possible  that  this  is  entirely  due  to  post-mortem  change, 
for  it  is  found  to  a  greater  or  less  extent  in  all  cases.  It  must  be 
partly  at  least  the  result  of  disorganization  which  occurred  during 
life.  The  condition  and  appearance  of  patients  in  the  last  stages  of 
typhoid  fever  are  more  like  those  of  dead  than  of  living  persons,  and 
this  suggests  that  there  may  be  death  of  the  tissues  while  the  life  of 
the  individual  still  continues.  Making  due  allowance  for  this  fact 
of  a  general  disorganization  of  tissue  in  typhoid  fever,  the  cord  often 
presents  lesions  which  are  the  results  of  disease  and  could  not  have 
been  produced  post  mortem.  In  such  cases  of  typhoid  fever  as  I  have 
examined  after  death,  the  cord  has  given  the  impression  that  it  had 
been  affected  by  inflammation.  The  axis  cylinders  of  the  nerves  in 
the  cord,  and  still  more  those  of  the  peripheral  nerves,  are  swollen. 
The  fibrous  envelopes  of  the  cord  also  appear  to  be  unnaturally 
adherent  and  perhaps  a  little  thickened.  These  changes  of  the  cord 
in  typhoid  fever  are  of  such  delicate  nature  that  it  is  difficult  to  be 
certain  of  their  existence,  but  there  cannot  be  any  doubt  that  they 
constitute  positive  disease.  The  subject  was  discussed  by  me  in  a 
paper  published  some  years  ago.* 

In  brain  syphilis  the  cord  was  found  to  be  fibroid  at  its  periphery, 
in  the  same  manner  as  it  has  been  said  is  sometimes  found  in  Bright's 
disease,  and  in  a  case  of  malignant  disease  of  the  abdominal  viscera, 
besides  bony  plates  in  the  pia-arachnoid,  this  same  thickening  and 
fibrosis  of  the  peripheral  portion  of  the  spinal  cord  were  found.  It 
seems  likely  that  the  fibrosis  in  this  latter  case  had  antedated  the  ma- 
lignant disease,  for  fibroid  material  is  usually  slowly  developed.  It  is 
impossible  to  say  that  fibrosis  had  no  influence  in  inducing  the  ma- 
lignant disease.  Certain  it  is  that  the  tissues  of  older  persons  are  much 
more  prone  to  malignant  disease  than  those  of  the  young,  and  fibrosis  is 
in  its  nature  a  disease  of  age.  Bony  plates,  as  they  are  called,  are  so 
commonly  present  in  the  membranes  of  the  spinal  cord  that  Wilks  and 
Moxon  f  say  that  "  half  the  population  at  thirty-five  have  a  few,"  and, 

*  The  Morbid  Anatomy  of  Typhoid  Fever.  The  Annual  Address,  delivered  before 
the  Philadelphia  Pathological  Society,  by  Arthur  V.  Meigs.  Medical  News,  November  15, 
1890. 

f  Pathological  Anatomy,  second  edition,  Philadelphia,  p.  247. 


THE   SPINAL   CORD.  169 

further,  that  "  it  is  a  great  and  rather  common  proof  of  ignorance  of 
the  spinal  cord  to  treat  them  in  a  post-mortem  examination  as  if  they 
bore  on  the  symptoms  of  the  case."  Although  it  is  true  that  they 
have  no  discoverable  influence  in  producing  symptoms  and  are  ex- 
ceedingly common,  it  is  important  to  keep  it  in  mind  that  they  must 
be  looked  upon  under  all  conditions  as  the  result  of  a  disease  process. 
Their  presence  is  an  evidence  that  the  fibrosis  which  is  inevitable  to 
the  advance  of  years  has  begun  in  the  individual  in  whom  they  are 
found,  and  that  therefore  his  bodily  condition,  which  at  one  time  was 
more  nearly  perfect,  has  somewhat  deteriorated. 

In  the  case  of  a  young  man  who  had  had  pulmonary  hemorrhage 
and  died  with  the  symptoms  of  acute  meningitis,  besides  a  large  cavity 
in  one  lung  and  other  lesions  of  tuberculosis,  the  condition  of  the 
spinal  cord  was  interesting.  There  was  nothing  like  miliary  tubercu- 
losis, nor  anything  else  to  show  that  the  meningitis  was  tubercular, 
although  the  lesions  in  the  lung  were  typical.  The  disease  of  the 
meninges  was  distinct,  there  being  extensive  infiltration  especially  of 
the  vessels  and  along  the  extensions  of  the  pia  mater  which  penetrate 
the  substance  of  the  cord.  Besides  this  condition  of  the  membranes, 
however,  the  cord  itself  was  greatly  involved,  there  being  much  de- 
struction of  the  nervous  tissue.  In  places  the  axis  cylinders  were 
swollen  and  in  other  places  had  disappeared  entirely ;  this  degener- 
ation was  most  extensive  in  the  posterior  columns.  It  is  instructive 
to  note  that  this  disease  of  the  cord  presents  a  precise  parallel  to  what 
has  been  described  as  so  common  in  chronic  diseases  involving  the 
thoracic  and  abdominal  viscera,  as  there  is  extensive  disease  of  the 
coverings — meningitis — and  at  the  same  time  great  degeneration  of 
the  organ  itself,  in  this  instance  the  cord.  The  question  cannot  be 
answered  whether  the  meningitis,  which  was  the  direct  cause  of  death 
in  a  man  who  had  also  pulmonary  tuberculosis,  is  to  be  looked  upon 
as  a  part  of  the  tubercular  process  or  was  an  accidental  intercurrent 
attack  of  different  nature.  If  only  tuberculosis  was  regarded  as  the 
result  of  tissue-change,  due  to  a  misdirected  growth  and  to  degenera- 
tion in  which  the  process  of  inflammation  plays  the  most  important 
part,  it  would  be  much  less  difficult  to  comprehend  the  combination 
in  the  same  individual  of  pulmonary  phthisis  and  acute  meningitis. 
Previous  to  the  introduction  of  the  germ  theory  of  disease,  which 
necessitates  the  belief  in  the  influence  of  an  infection  from  with- 
out in  all  cases  of  tuberculosis,  it  would  not  have  seemed  unreason- 
able to  suppose  that  both  the  pulmonary  disease  and  the  disease  of 


i7o  THE   ORIGIN   OF   DISEASE. 

the  cord  had  had  a  common  origin  in  some  tendency  which  as  yet 
defies  our  understanding.  This  would  not  seem  more  extraordinary 
ignorance  than  our  ignorance  of  the  reason  why  the  tubercle  bacillus 
grows  luxuriantly  in  the  lung  of  one  man  and  utterly  fails  to  grow 
in  another. 

In  all  the  diseased  spinal  cords  examined  by  me  the  peripheral 
nerves,  portions  of  which  are  always  included  with  sections  of  the 
cord,  were  found  to  have  participated  in  the  morbid  process.  The 
blood-vessels  also  are  commonly  involved,  often  being  thickened  in 
much  the  same  way  as  in  the  other  organs.  The  vessels  of  the  cord, 
however,  differ  somewhat  from  those  of  other  organs,  being  more 
delicate,  and  those  which  lie  in  the  membranes  around  the  cord 
present  the  further  difference  that  they  are  unsupported.  In  most 
tissues  and  organs  the  vessels  are  tubes  which  are  closely  surrounded 
by  a  solid  medium,  whereas  the  arachnoid  and  pia  mater  are  loose- 
meshed  and  serve  only  to  hold  the  vascular  tubes  in  position,  giving 
no  support  to  their  walls.  These  anatomical  conditions  make  the  ves- 
sels of  the  cord  different  from  those  of  other  organs,  and  they  seem  to 
me  less  liable  to  disease,  especially  to  great  thickening  of  their  walls, 
which  has  already  been  shown  to  be  so  very  common  in  the  blood- 
vessels of  the  thoracic  and  abdominal  viscera. 

At  present  meningitis  is  looked  upon  as  common,  and  the  diag- 
nosis is  frequently  made  by  physicians  who  recognize  several  forms 
of  the  disease.  On  the  other  hand,  from  the  clinical  stand-point 
myelitis  is  considered  to  be  rare.  In  none  of  the  cases  of  meningitis 
that  I  have  studied  with  the  microscope  have  the  lesions  been  con- 
fined to  the  membranes  and  exterior  of  the  cord,  but  in  each  in- 
stance there  has  been  evidence  of  inflammation  of  the  cord  itself, 
some  of  the  axis  cylinders  being  swollen  and  others  destroyed,  and 
parts  of  the  tissue  becoming  unusually  red  when  stained  with  car- 
mine, as  is  generally  the  case  in  inflammation.  This  view  having 
been  confirmed  by  the  pathological  evidence,  it  has  become  little 
short  of  a  certainty.  This  recalls  what  has  been  so  often  mentioned 
in  the  preceding  chapters,  the  strange  way  in  which  the  envelopes  of 
all  the  great  organs  of  the  body  become  inflamed  and  thickened  and 
adherent  to  surrounding  parts.  This  sometimes  occurs  when  the 
organs  themselves  are  greatly  diseased,  and  is  only  a  part  of  the  gen- 
eral process,  and  at  times  it  happens  when  the  organs  seem  healthy. 
The  precise  meaning  of  all  this  is  not  understood,  but  the  obser- 
vation makes  it  certain  that  the  surfaces  of  the  organs  and  their 


THE   SPINAL   CORD.  171 

» 
envelopes  are  the  most  vulnerable  parts  of  them,  and  are  much  more 

liable  to  disease  than  the  deeper  portions. 

Those  in  charge  of  institutions  for  the  care  of  the  insane  have  been 
reproached  with  having  done  little  or  nothing  to  advance  our  under- 
standing of  pathology.  So  little  was  known  of  the  pathology  of  in- 
sanity that  it  has  even  been  said  that  the  nervous  tissues  do  not 
undergo  physical  change  in  true  insanity.  Recently,  however,  there 
have  come  from  alienists  a  number  of  instructive  essays  directing 
attention  to  lesions  of  the  nervous  system  and  to  their  connection 
with  lesions  of  the  thoracic  and  abdominal  organs.  They  have  pointed 
out  that  Bright's  disease  and  pulmonary  phthisis  and  all  the  chronic 
bodily  diseases  are  often  connected  with  mental  unsoundness,  and 
that  lesions  of  the  nervous  system,  which  it  is  now  well  known  fre- 
quently exist,  are  often  connected  with  extensive  bodily  disease. 

Before  dismissing  the  subject  of  the  nervous  system  a  few  words 
must  be  added  concerning  the  brain.  Less  advancement  has  been 
made  in  the  pathology  of  the  brain  than  in  that  of  any  of  the  other 
organs.  As  has  already  been  said,  its  anatomy  is  so  complex  and  it  is 
so  delicate  as  to  be  more  difficult  to  examine  satisfactorily  than  any 
other  tissue.  The  grosser  forms  of  disease  to  which  it  is  subject,  such 
as  tumors  and  extensive  degenerations,  have  long  been  known,  and 
recently  great  advances  have  been  made  in  our  understanding  of  its 
anatomy  and  physiology.  The  difficulty,  however,  that  confronts  the 
pathologist  is,  in  the  first  place,  that  if  there  is  no  lesion  sufficiently 
gross  to  be  discoverable  by  the  unaided  eye  microscopical  study  is 
almost  hopeless.  The  size  of  the  brain  is  so  great  that  it  is  impossible 
to  examine  into  the  structural  condition  of  the  whole  of  it  with  the 
microscope,  and  therefore  all  that  can  be  done  is  to  study  portions  of 
it  taken  hap-hazard.  In  such  an  examination  it  might  well  happen 
that  the  portion  studied  would  prove  perfectly  healthy  while  if  the 
section  had  been  taken  from  another  region  close  by  extensive  dis- 
ease would  have  been  found.  Besides  this,  it  must  be  confessed  that 
our  comprehension  of  the  minute  anatomy  and  physiology  of  the 
brain  is  still  so  imperfect,  and  the  best  methods  of  microscopical 
technique  for  its  examination  still  leave  so  much  to  be  desired,  that 
often  it  is  impossible  to  be  certain  whether  minute  changes  are  the 
results  of  disease  or  are  due  to  faulty  preservation  or  preparation  of 
the  specimen.  My  own  studies  of  brain  tissue  might  have  been  more 
extensive,  but  they  have  led  to  one  or  two  observations  which  are 
worthy  of  mention.  In  the  case  of  death  from  meningitis  of  a  man 


172  THE   ORIGIN   OF   DISEASE. 

suffering  with  pulmonary  tuberculosis,  mentioned  in  connection  with 
the  discussion  of  the  spinal  cord,  it  was  found  that  there  was  cerebral 
as  well  as  spinal  meningitis.  Study  of  the  brain  with  the  microscope 
showed  that  just  as  there  was  myelitis  in  connection  with  the  spinal 
meningitis,  so  there  was  cerebritis  wherever  the  cerebral  meninges 
were  inflamed.  This  raises  again  all  the  questions  parallel  to  those 
which  were  discussed  in  connection  with  the  relations  of  spinal  menin- 
gitis and  myelitis. 

In  studying  a  case  of  brain  syphilis,  I  was  somewhat  surprised  to 
find  that  in  the  diseased  areas  the  blood-vessels  were  little  if  at  all  in- 
volved, and  that  the  disease  consisted  in  the  replacement  of  the  ordi- 
nary brain  tissue  by  morbid  fibrous  tissue.  The  blood-vessels  of  the 
brain  are  well  known  to  be  as  subject  to  disease  as  those  of  any  other 
organ.  The  disastrous  consequences  of  rupture  of  the  cerebral  vessels, 
which  causes  paralysis,  are  so  well  known  as  hardly  to  require  men- 
tion. It  is  my  opinion  that  in  apoplexy  ulceration  of  the  blood- 
vessels is  most  commonly  the  precedent  disease.  This  causes  slowly 
increasing  thinning  of  the  arterial  wall  until  perforation  takes  place 
without  strain  or  violence.  Apoplexy  is  not  usually  due  to  the  rup- 
ture of  a  stiffened  and  weak  vessel  caused  by  muscular  effort,  nor 
does  it  commonly  occur  because  the  heart  has  for  some  reason  driven 
the  blood  onward  with  unusual  force.  In  most  cases  neither  violence 
nor  effort  has  any  influence  in  causing  the  final  rupture  of  the  artery, 
for  generally  apoplexy  comes  on  while  the  individual  is  sitting  quietly 
or  even  lying  down.  The  process  is  one  of  ulceration  exactly  similar 
to  perforation  of  the  intestine  in  typhoid  fever  when  the  rupture  takes 
place  as  the  patient  lies  quietly  in  bed.  In  several  cases  of  cerebral 
apoplexy  which  have  come  under  my  notice  the  blood-vessels  were 
found  ulcerated  and  thinned,  and  in  one  the  vessel  at  the  seat  of 
hemorrhage  was  found  in  this  condition  of  ulceration,  with  the  open- 
ing in  it  "still  visible.  The  blood-vessels  of  the  brain  are  liable  to 
thickening  of  their  coats  in  a  manner  similar  to  that  which  is  so 
common  in  the  other  organs.  This  I  described  in  an  illustrated 
essay  published  some  years  ago.* 

*  A  Study  of  the  Arteries  and  Veins  in  Bright's  Disease,  by  Arthur  V.  Meigs.  Trans- 
actions of  the  College  of  Physicians  6f  Philadelphia,  June  6,  1888,  and  Medical  Record, 
July  7,  1888. 


CHAPTER    XIII. 

DIAGNOSIS    IN   CHRONIC    DISEASE. 

IT  is  not  intended  here  to  enter  upon  a  discussion  of  the  diag- 
nosis of  such  diseases  as  are  well  understood  and  have,  therefore, 
been  satisfactorily  classified,  but  to  deal  with  those  which  have  been 
under  consideration  in  the  preceding  pages.  It  has  been  indicated 
that  many  of  the  commonest  diseases,  if  not  most  of  them,  are  little 
understood  and  are  therefore  ill  classified,  and  that  for  these  reasons 
their  diagnosis  is  very  difficult.  Heretofore  diagnosis  has  been  nar- 
rowed by  the  prevalent  conception  that  disease  usually  lights  upon 
one  organ  or  another  and  confines  itself  to  a  restricted  district.  In 
the  endeavor  to  combat  this  error  it  has  been  repeated  so  often  as  per- 
haps to  make  it  a  wearisome  reiteration  that  disease  is  generally  wide- 
spread in  its  effects,  and  that  latent  and  chronic  disease  has  an  almost 
inconceivably  great  influence  in  starting  attacks  that  appear  purely 
acute  and  in  determining  their  course  and  outcome.  The  diagnosis 
of  chronic  disease,  and  the  relations  of  diseases  not  usually  supposed 
to  be  connected,  are  the  subjects  which  I  desire  to  discuss,  and  with 
these  will  be  included  such  observations  as  it  has  been  possible  to 
make  which  seem  to  show  that  any  of  the  ordinarily  accepted  doc- 
trines are  founded  on  error. 

From  the  study  of  what  has  been  named  Bright's  disease  more  has 
been  learned  in  the  direction  indicated  than  from  any  other  source. 
It  is  impossible  to  bestow  close  attention  upon  this  curious  condition 
without  noticing  that  at  one  time  or  another  it  has  been  made  to  in- 
clude symptoms  indicating  disease  of  every  organ  of  the  body,  and 
if  the  subject  is  pursued  to  the  post-mortem  room  the  fact  is  forced 
upon  the  attention  that  every  part  of  the  organism  is  liable  to  become 
the  subject  of  lesion.  Cases  usually  classed  as  chronic  organic  heart 
disease,  and  occasionally  those  of  chronic  disease  of  the  brain  and 
spinal  cord,  also  illustrate  the  fact  that  the  lesions  in  organic  disease 
are  widely  spread  through  the  body.  No  better  method  of  elucidating 
the  degree  of  accuracy  and  at  the  same  time  the  limitations  of  diag- 
nosis as  ordinarily  pursued  could  be  obtained  than  from  a  considera- 
tion of  a  suitable  illustrative  case.  In  this  way  may  be  shown  what 


174  THE   ORIGIN   OF   DISEASE. 

disease  was  thought  to  exist  during  life,  and  the  post-mortem  exam- 
ination can  be  used  to  verify  the  results,  showing  how  accurate  the 
diagnosis  was,  in  what  it  failed,  and  what  must  be  done  to  attain 
greater  exactitude  in  the  future.  The  case  which  will  be  narrated  was 
one  which  seemed  to  be  of  commonplace  nature,  and  nothing  but  the 
very  careful  and  thorough  study  post  mortem  made  it  so  interesting 
and  instructive.  In  the  hospital  in  which  the  man  died  the  case  is 
recorded  as  one  of  Bright's  disease.  A  number  of  the  illustrations 
which  have  been  included  with  the  discussion  of  disease  of  different 
organs  were  taken  from  this  case.* 

A  man  of  fifty-seven  years,  who  had  had  various  attacks  of  illness 
during  his  life  and  had  been  dissipated  but  had  as  a  general  thing 
enjoyed  good  health,  noticed  that  he  was  very  short  of  breath  on 
going  up-stairs.  This  was  about  six  months  before  his  death,  and  was 
the  first  warning  he  had  of  any  departure  from  his  usual  good  health. 
Soon  afterward  he  "  took  cold,"  his  feet  swelled,  there  was  difficulty 
of  breathing,  and  he  became  very  weak.  He  often  had  pain  in  the 
region  of  the  heart,  but  had  no  cough  or  urinary  or  bowel  disturbance. 
In  the  hospital  it  was  found  that  the  urine  contained  a  small  amount 
of  albumen  and  hyaline  casts.  The  radial  and  femoral  arteries  were 
stiff,  and  there  was  more  visible  pulsation  of  the  arteries  near  the 
surface  than  is  usual  in  healthy  persons.  The  cardiac  impulse  was 
diffuse,  but  not  of  great  force.  At  the  apex  of  the  heart  both  sounds 
were  distinct,  and  there  was  a  systolic  murmur.  In  both  the  pul- 
monary and  the  aortic  region  a  systolic  murmur  was  audible.  At  the 
bases  of  the  lungs  posteriorly  there  was  great  impairment  of  the 
percussion  resonance,  amounting  almost  to  dulness,  and  greater  on 
one  side  than  on  the  other.  There  was  almost  entire  absence  of 
breath-sounds  at  the  bases,  more  positive  on  the  side  which  was 
dull  on  percussion.  At  the  middle  portions  of  the  lungs  there  were 
some  crackles,  and  at  the  apices  the  sounds  were  natural.  At  places 
over  the  posterior  portions  of  the  lungs  percussion  caused  pain. 
There  was  no  increase  of  the  area  of  percussion  dulness  over  the 
liver,  and  in  the  region  of  the  usual  splenic  dulness  there  was  tym- 
pany.  The  abdomen  was  somewhat  full,  and  there  was  fluctuation. 
The  patient's  intelligence  continued  good,  but  the  dropsy  and  orthop- 
noea  increased,  and  he  became  extremely  restless  and  distressed. 
There  were  constant  pain  and  breathlessness,  to  such  a  degree  that  he 

*  Figs.  7,  28,  29,  36,  48,  49,  50,  68,  85,  89,  109,  127,  128,  129,  132,  and  133  were 
all  from  this  case. 


DIAGNOSIS   IN   CHRONIC    DISEASE.  175 

was  in  torture,  which  continued  until  his  death.  There  are  few  dis- 
eases in  which  death  is  more  painful  than  in  Bright's  disease  when 
the  final  illness  is  greatly  prolonged.  The  post-mortem  examination 
showed  the  heart  to  be  about  one  and  a  half  times  the  natural  size, 
and  the  tissue  exceedingly  hard  and  tough.  Upon  the  inner  surface 
of  the  ventricles  there  were  whitish  fibrous  spots  which  upon  section 
were  seen  to  be  about  one-sixteenth  of  an  inch  thick.  The  mitral 
valve  was  somewhat  thickened  and  its  cords  shortened,  allowing  less 
free  motion  than  natural.  The  aortic  valve-flaps  contained  small  de- 
posits of  chalk  which  somewhat  stiffened  them.  The  aorta  was  natural 
to  the  diaphragm,  but  the  abdominal  aorta  and  the  iliacs  were  very 
atheromatous  and  chalky.  The  vena  cava  and  iliac  veins  looked  nat- 
ural. The  lungs  were  everywhere  firmly  adherent.  On  section  they 
appeared  intensely  congested  and  in  places  were  nearly  solid.  Such 
portions  of  the  lungs  were  very  dark-colored.  The  pleura  was  greatly 
thickened.  The  abdominal  cavity  contained  a  large  amount  of  fluid. 
The  liver  was  rather  small,  and  weighed  two  pounds  and  six  ounces. 
It  was  firm  in  texture,  and  on  section  the  fibrous  tissue  seemed  in- 
creased in  quantity.  The  spleen  was  of  normal  size,  but  very  hard, 
and  its  capsule  exceedingly  thick.  The  walls  of  its  arteries  were  so 
much  infiltrated  with  chalk  that  they  were  stiff  like  bony  tubes.  The 
intestines  appeared  to  be  normal,  except  that  the  calibre  was  small 
from  contraction  and  the  gut  seemed  to  be  unusually  short.  The 
mesentery  and  greater  and  lesser  omentum  were  much  infiltrated  with 
chalky  masses,  so  that  they  were  snarled  and  twisted  out  of  shape.  In 
the  posterior  walls  of  the  abdominal  cavity  there  were  large  and  ex- 
tensive chalky  deposits.  The  kidneys  were  small,  firm,  and  dark-red 
in  color,  and  the  capsules  thick.  They  weighed  together  nine  ounces, 
and  appeared  to  be  not  more  than  two-thirds  the  natural  size.  There 
was  positive  but  not  very  great  increase  of  the  subarachnoid  fluid. 
The  carotid  and  vertebral  arteries  at  their  entrance  and  for  half  an 
inch  within  the  skull  were  thick  and  white.  The  vessels  of  the  dura 
mater  looked  thick.  The  brain-substance  appeared  normal.  The 
spinal  cord  looked  natural,  but  there  were  a  few  bony  plates  in  the 
posterior  portion  of  the  pia-arachnoid  in  the  dorsal  region.  There 
were  numerous  ecchymoses  of  the  skin  of  the  posterior  part  of  the 
body.  Many  sections  of  various  organs  and  tissues  were  cut  and 
examined  with  the  microscope,  and  they  demonstrate  an  extraordi- 
nary condition  of  disease,  when  it  is  recollected  that  the  case  was  one 
of  ordinary  Bright's  disease.  In  connection  with  the  illustrations  the 


176  THE   ORIGIN   OF   DISEASE. 

various  lesions  are  discussed  in  their  appropriate  places.  The  micro- 
scopical examination  demonstrated  extensive  disease  of  the  blood- 
vessels, disease  of  the  heart,  lungs,  liver,  spleen,  omentum,  mesentery, 
kidneys,  and  spinal  cord,  and  that  the  ecchymoses  of  the  surface  had 
resulted  from  the  escape  of  blood  into  the  skin  and  the  subcutaneous 
tissues.  The  utter  inadequacy  of  a  diagnosis  of  Bright's  disease  of 
the  kidney  in  such  a  case  as  descriptive  of  the  real  conditions  is  so 
plain  that  it  must  be  evident  to  any  one  who  has  carefully  con- 
sidered the  subject.  Sometimes  such  a  death  seems  like  the  natural 
result  of  the  advance  of  years,  the  machinery  wearing  out  simply 
because  it  is  too  old ;  or,  again,  it  is  as  if  premature  old  age  came 
upon  the  patient,  or  perhaps  he  is  worn  out  by  dissipation,  or  by 
some  physical  labor  so  severe  that  it  necessarily  speedily  exhausts 
his  vital  forces  and  produces  physical  disorganization.  In  order  to 
draw  the  full  measure  of  profit  from  the  case  it  must  be  studied  from 
three  aspects, — the  clinical  history,  the  post-mortem  examination,  and 
the  microscopical  study  of  the  tissues.  The  case  would  have  been 
looked  upon,  if  the  symptoms  had  been  considered  in  the  ordinary 
way,  as  one  of  Bright's  disease,  and  all  the  symptoms  and  lesions 
grouped  around  the  kidney  as  the  point  of  origin.  The  beginning 
with  shortness  of  breath,  soon  followed  by  dropsy,  and  then  the 
discovery  of  albumen  and  casts  in  the  urine,  and  the  various  suc- 
ceeding events  in  the  history,  are  all  the  ordinary  ones  of  Bright's 
disease.  But  to  suppose,  because  the  kidney  was  contracted,  that 
the  disease  of  the  heart,  of  the  lungs,  of  the  blood-vessels,  and  the 
multitudinous  other  lesions  were  all  secondary  to  the  kidney  dis- 
ease is  without  any  warrant  in  reason.  Nothing  is  known  even  to 
show  that  the  disease  of  the  kidney  was  of  older  date  than  that  of  the 
other  organs,  and  the  succession  of  the  symptoms  would  indicate 
rather  the  contrary,  for  the  first  thing  noticed  was  shortness  of  breath 
on  going  up-stairs.  If  the  subject  be  looked  at  without  prejudice,  there 
is  nothing  really  known  to  show  that  dropsy  is  due  to  disease  of  the 
kidney.  The  multiplicity  of  lesions  in  such  cases  is  very  great,  and  it 
is  impossible  to  distinguish  the  direct  cause.  If  kidney  disease  does 
produce  dropsy  it  can  be  only  as  a  secondary  result  induced  by  some 
effect  which  the  kidney  is  able  to  produce  upon  the  more  distant  parts. 
But  to  return  to  that  which  more  directly  concerns  the  question  of 
diagnosis  and  what  may  be  learned  from  the  case  detailed.  There 
can  be  no  question  that  the  symptoms  indicated  clearly  the  existence 
of  disease  of  the  kidneys  and  of  the  heart  and  arteries.  The  lungs 


DIAGNOSIS   IN   CHRONIC  DISEASE.  177 

presented  diagnostic  features  usually  considered  to  denote  hypostatic 
congestion  or  oedema  or  a  slight  degree  of  hydrothorax.  There  was 
no  evidence  of  disease  of  the  liver,  and  percussion  of  the  splenic 
region  revealed  an  absence  of  even  the  usual  amount  of  dulness.  As 
has  been  said,  it  is  usual  to  set  up  the  kidney  disease,  which  is  easily 
ascertained  to  exist  if  albumen  and  casts  are  found  in  the  urine, 
as  the  central  point,  and  to  make  everything  else  turn  upon  this. 
Various  theories  have  been  brought  forward  to  show  how  the  kidney 
disease  produces  an  effect  upon  the  arterioles,  which  in  their  turn 
become  diseased  and  affect  the  heart.  Long  and  complicated  ex- 
planations have  been  written  showing  the  intimate  connection  of  the 
heart  and  the  kidney  through  the  circulation,  and  the  reaction  of  the 
one  upon  the  other,  and  how  disease  sometimes  has  its  origin  in  the 
heart  and  extends  to  the  kidney  and  again  arises  in  the  kidney  and 
extends  to  the  heart.  Some  of  these  theories  read  like  romance,  and 
are  so  beautiful  that  they  lead  one  astray,  until  the  time  arrives  to 
apply  them  in  diagnosis  and  to  fit  them  in  with  the  post-mortem 
lesions,  and  then  they  are  found  wanting,  for  nothing  is  known  to 
enable  one  to  discriminate  which  of  the  organs  first  became  diseased, 
or  that  the  disease  of  any  one  of  them  was  the  cause  of  disease  of 
another.  It  has  been  pointed  out  that  there  was  objective  evidence 
of  disease  of  the  kidneys,  heart,  arteries,  and  lungs,  and  this  was  so 
obvious  during  the  life  of  the  patient  that  it  was  easy  to  be  sure  of 
the  existence  of  disease  of  these  organs.  To  one,  however,  who  has 
carefully  considered  cases  of  this  nature,  and  has  had  a  large  expe- 
rience, the  clinical  history  tells  a  story  which  renders  it  possible 
to  make  a  much  more  comprehensive  diagnosis.  In  the  first  place, 
in  regard  to  the  blood-vessels,  they  are  so  universally  diseased  in 
Bright's  disease,  chronic  heart  disease,  and  all  allied  conditions  that 
it  is  always  safe  as  a  part  of  the  diagnosis  to  infer  that  they  will  be 
found  to  be  involved,  and,  as  a  general  thing,  extensively.  In  the  case 
related  there  was  objective  evidence  of  a  calcareous  condition  of  the 
radial  and  femoral  arteries,  and  this  made  the  existence  of  vascular 
disease  even  more  certain  than  would  have  been  the  case  if  these 
external  proofs  had  been  wanting,  as  frequently  occurs.  The  post- 
mortem examination  showed  how  extensive  this  involvement  of  the 
arteries  was.  In  the  chapter  upon  the  blood-vessels  it  has  been 
shown  how  very  frequently  they  are  involved,  and  that  there  is  every 
reason  for  supposing  that  the  vascular  changes  play  an  important  role 
in  chronic  disease  and  are  not  a  mere  incident  in  the  disease  of 


178  THE   ORIGIN   OF   DISEASE. 

the  various  organs  which  are  involved.  It  is  desirable  therefore,  in 
making  a  diagnosis,  to  try  to  form  an  estimate  of  the  condition  of  the 
blood-vessels,  for  beyond  doubt  they  have  an  important  influence  in 
chronic  disease.  It  has  been  pointed  out  in  the  chapters  on  the  dis- 
ease of  age  and  on  the  blood-vessels  that  disease  of  the  latter  is  the 
inevitable  result  of  the  advance  of  years,  and  frequently  occurs  at  all 
periods  of  life. 

The  kidneys  were  known  to  be  diseased  because  albumen  and 
casts  were  found  in  the  urine.  Although  many  curious  and  inter- 
esting things  in  regard  to  the  urine  have  been  discovered  of  recent 
years,  the  existence  of  albumen  and  casts  taken  in  connection  with 
the  presence  of  general  dropsy  and  the  signs  of  enlargement  of 
the  heart  still  indicates  positively  disease  of  the  kidneys,  if  there  is 
anything  positive  in  diagnosis.  When  this  has  been  said,  all  that 
there  is  to  tell  of  the  state  of  the  kidneys  has  been  told,  for  there  is 
no  way  to  ascertain  during  the  life  of  the  patient  what  is  the  nature  of 
the  disease,  or  even  whether  the  kidneys  are  enlarged  or  contracted. 
The  albumen  and  casts,  it  is  reasonable  to  believe,  indicate  the  exist- 
ence of  some  degree  of  inflammation  at  the  time  they  are  present  in 
the  urine.  The  various  theories  that  have  been  propounded  and 
around  which  classifications  have  been  built — that  the  passage  of  large 
amounts  of  urine  indicates  one  kind  of  disease  and  a  low  specific 
gravity  another,  that  this  kind  of  casts  denotes  one  form  of  disease 
and  that  another — are  useless,  and  will  be  found  not  to  yield  in- 
dications that  will  square  with  the  post-mortem  lesions.  After  much 
study  of  the  question,  there  is  only  one  thing  which  it  is  possible  for 
me  to  declare  with  any  degree  of  positiveness,  and  it  is  that  in  almost 
all  chronic  cases  in  which  the  kidney  is  involved  it  is  safe  to  diagnos- 
ticate a  greater  or  less  degree  of  morbid  fibrosis.  In  the  chapter  on 
the  kidney  the  various  forms  of  fibroid  deposit  have  been  illustrated, 
as  well  as  the  manner  in  which  it  has  its  origin. 

The  evidence  of  disease  of  the  heart  in  this  case  of  Bright's  disease 
was  most  positive,  for  in  addition  to  the  murmurs  which  were  de- 
tected, and  which  denoted  injury  of  the  valves,  the  impulse  of  the 
heart  was  diffuse,  although  not  very  forcible,  and  this  indicated  en- 
largement of  the  heart.  No  diagnostic  indication  can  be  more  posi- 
tive than  that  afforded  by  an  increase  of  the  area  of  the  cardiac 
impulse,  taken  with  the  peculiar  sensation  imparted  to  the  hand 
when  it  is  placed  over  the  heart,  when  it  is  of  increased  size.  One 
must  not  be  deceived  by  the  effect  produced  by  palpitation  and 


DIAGNOSIS   IN   CHRONIC   DISEASE.  179 

irregularity  of  the  cardiac  action.  The  heart  seems  to  beat  over 
an  increased  area  and  its  action  is  very  violent,  but,  ordinarily,  this 
does  not  last  a  long  time,  seldom  more  than  a  few  days,  whereas 
the  heaving  and  the  extended  impulse  caused  by  actual  enlargement 
are  always  present,  and  the  sensation  they  impart  to  the  hand  is 
generally  easy  to  recognize  after  it  has  been  frequently  felt.  There  is 
an  important  exception  to  the  rule  that  an  enlarged  heart  produces  a 
heaving  impulse  perceptible  over  an  increased  area, — namely,  that  in 
the  later  stages  of  disease,  when  death  is  near,  the  heart  becomes  so 
weak  that  even  when  it  is  of  enormous  size  it  fails  to  produce  such  an 
impulse.  It  frequently  occurs  that  patients  are  brought  to  hospitals  in 
the  last  stages  of  disease  and  the  physicians  are  called  upon  to  make  a 
diagnosis  without  knowing  anything  of  the  previous  condition  or  his- 
tory. Under  these  circumstances,  when  the  cardiac  action  is  very  feeble, 
it  is  often  impossible  to  form  any  just  estimate  of  the  size  of  the  heart. 
There  is  no  other  change  which  the  heart  can  undergo  more  impor- 
tant to  recognize  than  its  enlargement.  The  state  of  the  valves  is  in 
comparison  unimportant,  for  it  is  well  known  that  persons  suffering 
with  valvular  disease  often  live  out  their  natural  lives.  On  the  other 
hand,  when  the  heart  is  greatly  enlarged  life  is  seldom  very  pro- 
longed. It  has  been  pointed  out  in  the  chapter  upon  the  heart  that 
enlargement  of  it  means  disease  of  the  walls,  and  the  opinion  ex- 
pressed that  what  is  called  compensatory  hypertrophy  has  no  exist- 
ence. Various  forms  of  degeneration  of  the  heart-muscle  are  there 
also  illustrated  and  commented  upon. 

With  regard  to  the  lungs  in  the  case  under  consideration,  the  diag- 
nostic indications  that  they  were  diseased  were  sufficiently  plain.  It 
would  be  easy  to  say  that  the  results  of  percussion  and  auscultation 
indicated  the  existence  of  hypostatic  congestion  of  the  lungs,  and 
that  the  post-mortem  examination  showed  this  conclusion  to  be 
correct,  and  let  the  matter  rest  there ;  but  it  has  long  seemed  to  me 
that  the  lungs  take  a  very  important  part  through  the  course  of 
Bright's  disease,  that  they  generally  have  a  preponderating  influence 
in  causing  death  when  it  comes,  and  that  they  frequently  are  pointed 
out  by  the  clinical  history  as  the  organs  first  diseased.  It  has  been 
shown  that  the  failure  of  the  lungs  to  perform  their  function  is  the 
most  common  cause  of  death,  much  more  common  than  failure  of 
action  of  the  heart  or  of  the  brain,  the  only  other  organs  whose 
cessation  to  act  immediately  kills.  Such  being  the  case,  it  is  un- 
necessary to  explain  further  the  necessity  that  diagnosis  should  be 


i8o  THE   ORIGIN   OF   DISEASE. 

as  accurate  as  possible  in  order  to  ascertain  all  that  can  be  learned 
during  life  in  regard  to  disease  of  the  lungs.  The  case  under  con- 
sideration presents  the  opportunity  to  illustrate  diagnostic  points  of 
great  importance,  and  therefore  they  may  with  advantage  be  passed  in 
review  somewhat  at  length.  The  results  of  percussion  and  ausculta- 
tion were  such  as  are  most  common  in  Bright's  disease  or  in  any 
of  the  combinations  of  heart,  lung,  and  kidney  disease  which  in  prac- 
tice are  so  frequently  encountered.  They  were  as  follows :  dulness 
on  percussion  at  the  bases  of  the  lungs  posteriorly,  greater  on  one 
side  than  on  the  other,  and  at  the  areas  of  dull  percussion  almost  total 
absence  of  breath-sounds, — an  unnatural  silence.  At  the  middle  por- 
tions of  the  lungs  there  were  some  crackles,  and  at  the  apices  fairly 
good  breath-sounds.  No  note  was  made  of  the  condition  of  the  vocal 
resonance  and  fremitus,  which  was  an  oversight,  but  under  the  cir- 
cumstances both  the  fremitus  and  the  resonance  are  usually  greatly 
diminished  at  the  bases  posteriorly  corresponding  to  the  area  of  dul- 
ness. This  condition  has  been  so  frequently  found  by  me  in  other 
similar  cases  as  to  satisfy  me  that,  if  a  note  had  been  made  of  those 
diagnostic  features,  the  vocal  resonance  and  fremitus  would  have  been 
found  diminished.  One  other  point  was  mentioned  which  is  of  great 
importance,  although  it  seems  a  little  thing :  there  was  pain  on  per- 
cussion. Dulness  on  percussion  at  the  bases  of  the  lungs,  weakness 
or  absence  of  the  breath-sounds,  and  diminished  vocal  resonance  and 
fremitus  are  commonly  accepted  as  the  indications  of  hydrothorax. 
In  this  case  there  was  none.  Long  experience  with  cases  of  this  de- 
scription has  forced  me  to  the  conclusion  that  it  is  an  error  to  believe 
that  this  combination  of  physical  signs  necessarily  indicates  the  pres- 
ence of  fluid  in  the  pleural  sacs.  I  am  convinced  they  are  more  fre- 
quently produced  by  disease  of  the  lung  itself.  It  is  usually  taught, 
and  is  true,  that  when  the  lung  is  solid  there  are,  with  the  dulness 
on  percussion,  an  increase  of  the  vocal  fremitus  and  resonance,  and 
bronchial  breathing.  On  the  other  hand,  little  is  said  and  still  less 
commonly  taught  of  the  physical  signs  which  should  be  expected 
to  be  present  when  the  lung  is  in  such  a  condition  as  in  the  case  under 
discussion,  which  is  the  state  most  common  in  Bright's  disease  and 
toward  the  later  stages  in  most  chronic  diseases.  Examination  both 
macroscopically  and  with  the  microscope  of  a  great  many  such  lungs 
has  shown  me  that  there  is  a  combination  of  blood-corpuscles,  exu- 
date-cells,  and  fluid  in  varying  quantities  in  the  air-sacs.  Those  who 
have  examined  many  such  lungs  after  death  will  recollect  their  soggy 


DIAGNOSIS   IN   CHRONIC   DISEASE.  181 

condition,  how  freely  fluid  runs  from  them  when  they  are  cut,  and 
their  dark  bluish-black  color  like  that  of  clots  of  venous  blood.  When 
examined  with  the  microscope  large  areas  are  found  in  which  the 
air-sacs  are  rilled  with  exuded  blood-corpuscles  or  with  amorphous 
material  that  was  evidently  mingled  with  liquid  or  semi-gelatinous 
serum,  such  as  runs  or  can  be  squeezed  from  the  lung  when  it  is  cut. 
Commingled  with  all  this  unnatural  material  filling  the  air-sacs  is 
generally  to  be  seen  a  greater  or  less  number  of  the  large  cells  called 
exudate-cells.  Such  lungs  give  physical  signs  identical  with  those 
caused  by  the  effusion  of  liquid  into  the  pleural  sacs,  and  it  is  often 
impossible  clinically  to  distinguish  which  of  the  two  conditions  is 
present,  or  whether,  as  often  happens,  the  two  coexist.  It  seems  no 
more  than  might  have  been  expected,  when  one  stops  to  consider,  that 
liquid  in  the  pleural  sacs  and  liquid  in  the  lung  itself  should  produce 
identical  physical  signs,  and  the  conditions  called  oedema  of  the  lung 
and  hypostatic  pneumonia  are  simply  the  results  of  the  effusion  of 
liquid  or  semi-liquid  material  into  the  air-spaces  of  the  lungs.  The 
purpose  of  all  that  has  just  been  said  is  to  direct  attention  to  the  fact 
that  it  is  a  diagnostic  error  to  attribute  to  hydrothorax  the  combina- 
tion of  physical  signs  mentioned.  Although  a  small  amount  of  fluid 
is  sometimes  present  in  the  pleural  sacs,  oftener  there  is  none,  and 
even  when  there  is  some  pleural  effusion  the  lung  partakes  in  the  dis- 
ease process,  liquid  having  escaped  into  the  air-sacs.  For  all  practical 
purposes  there  is  no  such  thing  possible  as  a  simple  hydrothorax  as  a 
complication  of  Bright's  disease,  the  lung  being  always  to  a  greater 
or  less  degree  involved  also.  In  diagnosis,  therefore,  it  is  always  safe 
to  infer,  if  it  be  ascertained  that  there  is  fluid  in  the  pleural  cavity,  that 
the  lung  partakes  in  the  process  and  is  not  simply  forced  aside  and 
compressed  by  the  liquid.  Another  physical  sign  which  existed  and 
has  been  said  to  be  of  importance  was  pain  on  percussion.  This  sign 
will  be  found  to  indicate  almost  infallibly  the  presence  of  pleurisy. 
Some  degree  of  pleuritic  inflammation  and  adhesion  is  almost  univer- 
sally an  accompaniment  of  chronic  disease  of  the  lung,  and  therefore 
it  might  be  said  that  it  may  be  inferred  to  exist  without  there  being 
any  direct  sign  to  indicate  it.  The  examination,  however,  of  many 
cases  has  shown  me  that  when  there  is  marked  pain  on  percussion 
the  pleural  inflammation  is  extensive.  It  should  be  remembered  that 
in  the  case  under  consideration  the  pleural  adhesions  were  universal 
and  the  pleura  was  greatly  thickened.  In  consumption,  as  well  as  in 
ordinary  inflammatory  affections  with  the  lung  involved,  the  presence 


1 82  THE   ORIGIN   OF  DISEASE. 

of  pain  on  percussion  will  be  found  to  be  an  important  diagnostic  sign 
of  extensive  pleurisy  and  pleuritic  adhesions. 

Much  more  might  be  said  of  the  diagnosis  of  disease  of  the  lungs, 
particularly  in  regard  to  the  erroneousness  of  the  prevalent  belief  that 
in  cases  of  pneumonia  the  vocal  resonance  and  fremitus  are  generally 
increased.  If  the  term  pneumonia  is  made  to  include  all  the  ordinary 
inflammations  of  the  lungs,  the  vocal  resonance  and  fremitus  are  di- 
minished in  the  majority  of  cases.  There  is  only  one  form  of  pneu- 
monia which  causes  increase  of  the  vocal  resonance  and  fremitus,  the 
form  which  produces  hepatization,  in  which  the  lung  is  unnaturally 
hard  and  tends  to  be  dry.  Most  of  the  cases  of  pneumonia  or  inflam- 
mation of  the  lungs  that  are  encountered  are  not  of  this  variety.  The 
lung  is  found  to  be  here  and  there  solid,  but  scattered  through  the 
solid  portions  are  sacs  still  filled  with  air,  so  that  often  no  part  of 
the  lung  will  sink  in  water.  The  material  filling  the  air-sacs  can  be 
squeezed  out  to  a  great  extent  by  pressure  with  the  fingers,  and  the 
tissue  does  not  tear  easily,  as  hepatized  lung  does.  Examination  with 
the  microscope  shows  the  material  in  the  air-sacs  to  be  a  mixture  of 
blood-corpuscles,  exudate-cells,  amorphous  material  which  is  visible, 
and  other  matter  which  appears  as  empty  space,  being  unstained. 
There  is  generally  no  fibrin  to  be  seen  under  these  circumstances. 
The  physical  signs  produced  by  this  form  of  lung-inflammation  are 
impairment  of  the  percussion  sound,  but  not  flatness,  feebleness  of 
the  respiratory  sounds,  but  no  bronchial  breathing,  and  diminished 
vocal  fremitus  and  resonance.  The  conditions  are  rather  negative 
than  positive,  for  often  both  lungs  are  involved  and  therefore  a  good 
lung  cannot  be  compared  with  a  diseased  one.  There  is  frequently 
only  slight  impairment  of  the  percussion  resonance,  and  as  this  is 
on  both  sides  there  is  nothing  to  compare,  and  it  is  therefore  hard 
to  be  sure  of  it.  When  the  breath-sounds  are  listened  for,  there 
is  a  curious  silence,  and  it  is  difficult  to  determine  whether  this  is 
because  sounds  cannot  be  produced  or  because  the  patient  will  not 
breathe,  and  then,  perhaps,  the  vocal  resonance  and  fremitus  seem  to 
be  diminished.  Such  a  condition  is  of  frequent  occurrence  in  prac- 
tice, and  it  is  as  much  a  pneumonia  which  will  occasion  fever  and  take 
away  the  strength  and  force  the  patient  to  go  to  bed,  as  is  the  form  in 
which  the  lung  becomes  hepatized  and  all  the  classical  signs  that  can 
be  elicited  by  percussion  and  auscultation  are  present.  This  theme  of 
the  diagnosis  of  pneumonia  could  be  pursued  to  much  greater  length, 
but  it  might  lead  too  far  from  our  subject. 


DIAGNOSIS   IN   CHRONIC   DISEASE.  183 

The  case  selected  as  a  type  has  now  been  discussed  so  far  as 
concerns  the  objective  signs  of  disease  brought  to  light  by  the  clinical 
history  and  physical  examination.  These  made  evident  that  there  was 
disease  of  the  heart  and  of  the  blood-vessels,  of  the  lungs  and  of  the 
kidneys.  No  other  direct  evidence  of  disease  existed,  and  the  case 
might  have  been  called  Bright's  disease,  and  its  study  pursued  no 
further,  it  being  assumed  that  the  process  had  its  origin  in  the  kidney 
and  thence  extended,  the  involvement  of  the  other  organs  being  a 
direct  consequence  of  the  disease  of  the  kidney.  It  has  been  said  that 
the  theories  which  make  disease  of  the  kidney  the  cause  of  so  much 
disease  of  other  organs  have  no  firm  foundation,  and  from  the  diag- 
nostic stand-point  totally  fail  to  explain  most  of  the  common  phe- 
nomena of  Bright's  disease.  Bright's  disease  is  now  well  known  to 
include  extensive  involvement  of  other  organs  besides  the  kidneys, 
and  should  no  longer  be  classed  simply  as  a  disease  of  the  kidney. 
It  is  possible  in  diagnosis  to  go  far  beyond  that  which  can  be  known 
from  objective  signs  and  symptoms  alone.  Much  may  be  inferred 
as  a  matter  of  general  principle  of  what  must  occur  in  organs  which 
yield  no  external  sign  recognizable  during  life.  The  physician  who 
would  have  the  most  comprehensive  grasp  upon  his  cases  must  keep 
ever  in  mind  that  after  all  available  methods  of  diagnosis  have  been 
exhausted  there  still  often  is  disease  which,  having  eluded  discovery 
during  life,  was  not  recognized  at  the  post-mortem  examination,  and 
was  brought  to  light  only  by  the  use  of  the  microscope.  The  case 
under  consideration  illustrates  this.  The  history  shows  that  the 
hepatic  dulness  was  not  increased,  and  that  there  was  tympanitic  reso- 
nance in  the  area  of  ordinary  splenic  dulness.  It  has  been  again  and 
again  mentioned  in  the  previous  chapters  that  fibrosis  is  an  essential 
part  of  chronic  Bright's  disease,  and  that  it  is  seldom  confined  to  a 
few  organs,  but  is  usually  widely  spread.  In  such  cases,  therefore, 
it  is  a  fair  diagnostic  inference  to  make  that  when  the  heart,  blood- 
vessels, lungs,  and  kidneys  are  diseased  the  liver  and  spleen  will  not 
escape.  Although  there  was  no  external  diagnostic  evidence,  it  was 
safe  to  predict  that  the  liver  and  spleen  would  be  found  diseased. 
The  post-mortem  and  microscopical  examination  showed  this  to  be 
the  case,  and  the  illustrations  (Figs.  85  and  89)  demonstrate  the 
fibrosis  of  both  of  those  organs.  In  interpreting  the  results  obtained 
from  physical  examination  of  the  liver  and  spleen  it  must  be  remem- 
bered that  percussion  and  palpation,  which  are  the  only  available 
methods,  yield  at  best  very  imperfect  indications  and  give  no  informa- 


184  THE   ORIGIN   OF   DISEASE. 

tion  whatever  in  regard  to  the  slighter  changes.  When  the  liver  is 
greatly  enlarged  or  very  small  it  is  often  possible  during  .life  to  be 
pretty  certain  of  it,  but  when,  as  happened  in  the  case  under  dis- 
cussion, the  reduction  in  size  is  very  slight,  it  is  impossible  to  find  this 
out,  although  the  organ  may  be  greatly  diseased,  as  was  indeed  the 
fact.  The  spleen  being  of  small  size  and  hidden  within  the  cage  of 
the  thorax,  information  in  regard  to  its  size  obtained  from  physical 
examination  is  still  less  reliable.  In  the  type  case  there  was  no 
splenic  dulness,  which  would  have  seemed  to  indicate  that  the  organ 
was  small,  and  yet  post  mortem  it  was  found  to  be  of  normal  size  and 
greatly  diseased.  Even  if  it  had  been  possible  during  life  to  know  that 
it  was  of  normal  size,  the  fact  that  it  was  diseased  would  still  have 
remained  undiscovered.  The  lesson  which  it  is  intended  to  emphasize 
by  what  has  been  said  of  the  liver  and  spleen  is  that  all  the  available 
methods  of  physical  diagnosis  should  be  employed,  but  that  it  is  still 
more  important  to  remember  the  habit  of  chronic  disease  to  produce 
wide-spread  effects,  and,  therefore,  that  more  may  often  be  learned  of 
the  condition  of  these  organs  from  general  inference  of  what  must 
occur  if  the  blood-vessels,  heart,  lungs,  and  kidneys  are  diseased  than 
could  be  learned  directly  from  percussion  and  palpation. 

The  second  fact,  that  important  lesions  may  exist  and  fail  to  reveal 
their  presence  by  clinical  symptoms  and  elude  discovery  at  the  post- 
mortem examination,  to  be  demonstrated  only  by  the  use  of  the 
microscope,  is  illustrated  by  what  was  found  in  the  spinal  cord.  There 
were  no  clinical  symptoms  of  disease  of  the  nervous  system,  and  at 
the  post-mortem  examination  the  brain  and  spinal  cord  appeared  to  be 
normal.  The  illustrations  (Figs.  127,  128,  and  1 29)  show  how  false 
would  have  been  the  conclusion  that  they  were  really  healthy.  It 
is  unnecessary  here  to  discuss  the  nature  of  the  disease,  for  this  has 
already  been  done  in  its  appropriate  place  in  connection  with  the  illus- 
trations in  the  chapter  on  the  spinal  cord. 

What,  then,  are  the  lessons  which  should  be  learned  from  the  case 
which  has  been  related  and  commented  upon  from  so  many  points  of 
view  ?  It  emphasizes  in  the  most  positive  way  the  inadequacy  of  the 
view  that  Bright's  disease  is  essentially  a  disease  of  the  kidney.  This 
was  discussed  by  me  in  an  essay  published  some  years  ago.* 

There  are  three  salient  points  to  be  kept  in  mind  in  diagnosis : 

*  A  Study  of  the  Arteries  and  Veins  in  Bright's  Disease,  by  Arthur  V.  Meigs.  Trans- 
actions of  the  College  of  Physicians  of  Philadelphia,  1888,  and  Medical  Record,  July  7, 
1888. 


DIAGNOSIS   IN   CHRONIC    DISEASE.  185 

first,  all  available  methods  of  investigation  must  be  employed  which 
can  directly  indicate  disease  of  the  organs,  and  these  must  be  brought 
to  bear  upon  as  many  of  the  organs  as  possible ;  second,  owing  to  the 
habit  of  chronic  disease  to  produce  wide-spread  effects,  it  is  generally 
possible  to  draw  inferences  of  the  existence  of  disease  which  reveals 
itself  by  no  external  indication ;  and,  third,  owing  to  this  same  habit 
of  chronic  disease  to  spread  itself  over  a  great  extent  of  the  bodily 
territory,  there  are  often  lesions  which  the  microscope  alone  reveals, 
they  having  made  no  sign  by  clinical  symptoms,  nor  been  visible  to 
the  naked  eye  at  the  post-mortem  examination. 

The  diagnostician  who  shuts  his  eyes  to  the  revelations  of  pathology 
during  the  last  thirty  years, — to  all  that  has  been  learned  since  Gull 
and  Sutton  put  forth  their  classic  observations  on  "  arterio- capillary 
fibrosis," — and  continues  to  regard  disease  from  the  earlier  stand-point, 
must  fail  to  understand  the  chronic  cases  that  have  the  misfortune  to 
fall  into  his  hands.  The  puzzle  in  diagnosis  often  encountered,  to  de- 
cide which  is  the  primary  disease,  when  it  has  been  ascertained  that 
there  is  in  a  given  case  organic  disease  of  the  heart,  lungs,  and  kidneys, 
is  frequently  insolvable.  The  name  Bright's  disease  has  now  long 
been  given  to  cases  with  albumen  and  casts  in  the  urine  and  dropsy. 
With  these  symptoms  it  has  been  found,  as  time  has  passed,  that  there 
are  generally  associated  disease  of  the  blood-vessels,  of  the  heart,  and 
of  the  lungs,  and  occasionally  convulsions  called  uraemic,  and  some- 
times insanity.  Close  scrutiny  reveals  that  at  one  time  or  another 
disease  of  almost  every  one  of  the  organs  and  the  symptoms  of  every 
known  form  of  chronic  disease  are  found  associated  with  what  the 
puzzled  diagnostician  cannot  escape  from  calling  Bright's  disease. 
The  pathological  condition  common  to  all  the  organs  thus  invaded  is 
an  increase  of  their  fibrous  tissue,  and  with  this  vascular  disease  is 
almost  universally  associated.  One  of  two  things  is  almost  certain  to 
happen:  the  term  Bright's  disease  will  be  made  to  include  a  much 
more  extensive  range  of  disease  than  it  originally  covered,  or  it  will 
disappear  from  the  accepted  nomenclature.  The  latter  is  much  the 
more  likely  to  occur,  although  it  will  never  be  forgotten  that  Bright's 
discoveries  marked  an  important  advance  in  medicine.  For  the  diag- 
nostician cases  of  chronic  disease  with  involvement  of  many  organs 
present  great  difficulty  so  long  as  his  work  continues  hampered  by 
the  older  views  of  the  subject ;  to  reach  a  position  where  a  reasoning 
mind  can  rest  with  any  degree  of  satisfaction  it  is  necessary  to  cast 
aside  many  theories  that  have  been  long  received,  and  to  give  up 


186  THE   ORIGIN   OF   DISEASE. 

comfortable  explanations  of  things  that  are  hard  to  understand.     The 
state  of  knowledge  at  the  present  time  is  about  this :  the  wide-spread 
disease  of  the  tissues  and  organs  in  the  conditions  under  discussion 
is  well  known,  and  it  has  been  ascertained  that  the  pathological  lesions 
which  form  an  invariable  accompaniment  are  varying  forms  and  de- 
grees of  fibrosis  and  vascular  disease.      With  the  progress  of  time 
and  the  advance  of  knowledge  so  much  has   been  included  by  the 
name  Bright's  disease  that  the  term  will  no  longer  cover  all  that  it  is 
attempted  to  place  under  it.     It  is  manifest  that  to  talk  of  disease  of 
the  kidney  is  quite  aside  from  the  facts  in  many  cases,  for  often  the 
kidney  does  not  bear  any  important  part.     Of  the  ulterior  causes  of 
chronic  disease  something,  but  by  no  means  all,  is  known.     There 
can  be  no  doubt  that  the  passage  of  time  produces  it,  the  fibrosis 
which  is  inevitable  to  age  coming  sooner  or  later  in  every  one  not 
cut  off  in  some  accidental  way,  and  with  the  fibrosis   come  those 
forms  of  inflammation  to  which  morbidly  fibroid  tissues  are  prone ; 
the  combination  of  fibrosis  and  inflammation  constitutes  the  disease. 
It  is  equally  certain  that  dissipation,  unhealthy  modes  of  living,  and 
what  appears  to  be  an  inherited  disposition  to  premature  decay  can 
produce  the  same  or  very  similar  effects  even  in  young  persons.     The 
relations  of  other  forms  of  disease,  which  at  first  sight  appear  to  have 
nothing  in  common  with  the  ordinary  chronic  diseases,  have  been  dis- 
cussed in  some  of  the  preceding  chapters.     The  purpose  of  the  last 
few  pages  has  been  to  emphasize  the  statement  that  the  diagnostician 
must  learn  to  regard  such  conditions  as  that  presented  by  the  type 
case  of  Bright's  disease  which  was  given,  and  many  cases  of  disease 
of  other  of  the  great  organs,  as  but  the  varying  expressions  of  the 
same  process.      Although  this  strange  and  wide-spread  process  is 
very  imperfectly  understood,  enough  is  known  to  make  it  necessary  to 
acknowledge  its  existence.     One  chapter  has  been  devoted  to  the  cita- 
tion of  the  facts  showing  that  there  is  such  a  thing  as  the  disease  of 
age ;  again,  it  has  been  argued  that,  owing  to  the  operation  of  various 
causes,  some  of  which  were  named,  there  arises  a  state  of  disease 
which  was  likened  to  age  in  youth.     It  has  been  pointed  out  that 
both  the  last-mentioned  states  are  recognized  by  the  diagnostician  as 
Bright's  disease.     Pathology  gives  the  information  that  the  lesion  in- 
variably present  in  all  is  fibrosis.     It  seems,  therefore,  only  reasonable 
to  call  the  disease  fibrosis,  with  the  reservation  that  it  is  certain  that 
final  knowledge  has  not  yet  been  even  approached,  for  there  must  be 
some  great  underlying  cause  which  still  remains  hidden. 


DIAGNOSIS   IN   CHRONIC   DISEASE.  187 

There  are  other  states  of  disease  which  it  is  necessary  for  the 
clinician  to  recognize  and  classify  by  diagnosis.  It  commonly  hap- 
pens that  cases  are  met  with  in  which  the  history  and  physical  signs 
appear  to  indicate  clearly  that  the  heart  was  first  diseased  and  after- 
ward the  other  organs  became  involved.  Often,  as  such  a  case  pro- 
gresses it  presents  the  entire  clinical  picture  of  Bright's  disease,  but 
neither  albumen  nor  casts  at  any  time  appear  in  the  urine.  It  even 
happens  that  the  urine  is  passed  in  normal  quantity  and  is  of  normal 
specific  gravity.  What  diagnosis  is  to  be  made  under  these  circum- 
stances ?  It  has  occurred  to  me  a  number  of  times  in  such  instances 
to  find  at  the  post-mortem  examination  the  kidneys  contracted  and 
cystic, — types  of  fibrosis.  Several  important  lessons  are  taught  by 
this.  .  It  is  a  fair  diagnostic  inference  that  the  kidneys  will  be  more  or 
less  fibroid  when  the  other  great  organs  are  so  diseased,  and  this  will 
be  found  to  be  seldom  erroneous.  The  inference  is  precisely  parallel 
to  that  which  it  has  already  been  pointed  out  may  be  made  in  regard 
to  the  liver  and  spleen  in  the  absence  of  objective  evidence  of  their 
being  diseased.  The  kidney  is  frequently  diseased  when  there  is  no 
evidence  of  it  to  be  obtained  from  examination  of  the  urine,  and  this 
is  an  important  fact  to  be  kept  in  mind  in  diagnosis.  Such  a  case 
constitutes  another  link  in  the  chain  of  proof  that  the  term  Bright's 
disease  has  grown  to  cover  an  enormous  extent  of  disease,  and  that 
there  is  every  reason  to  suppose  the  kidney  plays  a  very  minor  role, 
being  only  more  important  than  the  liver  and  the  spleen,  and  im- 
measurably less  so  than  the  heart  and  the  lungs,  and  occasionally  the 
brain.  In  the  same  way  that  it  happens  that  the  heart  is  the  first 
organ  to  be  attacked  in  cases  which  subsequently  present  the  clinical 
picture  called  Bright's  disease,  it  frequently  occurs  that  the  lung  is 
first  involved.  An  attack  of  catarrhal  pneumonia  or  a  predisposition 
to  take  cold,  with  numerous  colds  during  the  course  of  a  year  or  two, 
in  a  person  previously  perfectly  healthy  is  frequently  the  opening  to  a 
chronic  illness  which  sooner  or  later  takes  the  form  of  Bright's  disease 
and  ends  in  death.  Jaundice  or  other  disease  of  the  liver  may  mark 
the  beginning  of  such  chronic  disease.  From  the  point  of  view  of 
diagnosis  such  cases  are  sometimes  very  puzzling,  and  were  formerly, 
when  Bright's  disease  was  looked  upon  as  essentially  a  disease  of  the 
kidney,  more  so  than  at  present,  since  a  more  comprehensive  view  is 
now  taken.  In  these  combinations  of  disease  the  diagnosis  must  be 
pursued  along  the  lines  already  indicated,  all  methods  of  physical  ex- 
amination being  exhausted  to  ascertain  the  condition  of  as  many  of 


1 88  THE   ORIGIN   OF   DISEASE. 

the  organs  as  possible,  and  from  this  inferences  drawn  in  regard  to 
disease  of  parts  that  give  no  external  sign ;  and  it  must  be  remem- 
bered that  even  after  this  has  been  done  there  will  still  remain  lesions 
that  are  discoverable  only  by  microscopical  examination. 

Perhaps  the  most  extraordinary  clinical  picture  is  that  presented 
when  the  nervous  system  is  first  attacked.  This  subject  has  already 
been  mentioned  in  the  chapter  on  the  spinal  cord.  Of  more  recent 
years  a  number  of  essays  have  appeared,  written  by  alienists,  direct- 
ing attention  to  the  connection  of  insanity  with  Bright's  disease. 
This  goes  to  show  that  the  brain  as  well  as  all  the  other  great 
organs  is  liable  to  suffer  in  the  course  of  chronic  disease,  and  that 
it  as  well  as  any  of  the  others  may  be  the  first  to  be  attacked.  It 
is  not  a  rare  occurrence  in  practice  that  insanity  is  developed  in  the 
course  of  Bright's  disease,  and  alienists  now  allege  that  the  two 
frequently  have  some  connection.  This  makes  it  highly  probable 
that  the  fibrosis  and  vascular  disease  which  are  found  widely  ex- 
tended in  the  bodily  organs  will  soon  be  discovered  to  be  as  fre- 
quently present  in  the  brain.  It  has  happened  to  me  a  number  of 
times  to  see  cases  in  which  disease  of  the  spinal  cord  was  inex- 
tricably mingled  with  general  chronic  disease.  In  some  of  them 
there  was  clinical  evidence  of  disease  of  other  organs  before  that  of 
the  cord  manifested  itself,  but  in  two  the  spine  was  the  first  organ  to 
show  itself  to  be  diseased,  and  there  were  other  clinical  phenomena  of 
such  unusual  or  obscure  nature  as  to  make  one  of  the  cases  worthy 
of  discussion  at  some  length. 

A  man  who  died  at  seventy  was  throughout  his  life  very  healthy. 
Twelve  years  before  his  death  he  had  an  attack  of  catarrhal  pneu- 
monia following  exposure,  but  recovered  completely.  Between  two 
and  four  years  afterward,  and  so  gradually  that  a  more  exact  period 
cannot  be  fixed,  he  began  to  fail.  This  took  the  form  of  weakness 
of  the  legs,  so  that  walking  was  disagreeable,  and  then  difficult.  His 
gait  was  uncertain  and  shuffling,  the  feet  not  being  lifted  naturally 
from  the  ground.  This  condition  of  the  legs  increased  until  he  could 
walk  but  little,  and  occasionally  had  falls  owing  to  slight  causes ;  then 
he  gave  up  walking  almost  entirely,  and  at  last  was  unable  to  walk 
without  assistance.  Upon  several  occasions  he  was  impelled  to  run 
(a  symptom  not  uncommon  in  spinal  disease),  and  once  or  twice  fell, 
at  other  times  saving  himself  by  seizing  some  fixed  object,  which  he 
held  until  his  equilibrium  was  regained.  His  gait  was  neither  ataxic 
nor  spastic,  but  rather  one  of  mistrust  of  his  power  of  equilibration, 


DIAGNOSIS   IN   CHRONIC   DISEASE.  189 

the  steps  being  short  and  shuffling.  The  sense  of  touch  was  not 
impaired,  and  the  reflexes  of  the  tendons  of  the  patellae  were  absent. 
Three  years  before  his  death  all  the  muscles  of  both  lower  extremi- 
ties were  found  to  react  to  the  slowly  interrupted  faradic  current. 
Of  the  left  leg  the  reaction  to  the  rapidly  interrupted  current  was 
very  poor,  and  to  the  slowly  interrupted  current  much  more  feeble 
than  the  reaction  of  the  right  leg.  The  muscles  were  weak,  small, 
and  flabby.  More  than  once  he  lost  control  of  his  rectal  sphinc- 
ter. The  bladder  performed  its  function  naturally.  The  urine  was 
examined  occasionally  in  various  years,  and  neither  albumen  nor  casts 
were  found,  and  when  the  specific  gravity  was  taken  it  was  normal, 
or  above  the  normal.  The  mental  as  well  as  the  bodily  condition 
seemed  involved  in  the  process  of  decay.  He  was  never  in  the  slight- 
est degree  insane,  but  became  crotchety,  irritable,  and  mentally  in- 
efficient. At  times  the  pulse  was  very  irregular  and  the  digestion 
disordered,  but,  as  a  general  thing,  through  the  whole  of  the  eight 
or  ten  years  of  illness  the  bodily  health  was  fairly  good.  Physical 
examination  never  developed  signs  of  disease  of  any  of  the  organs. 
For  some  months  or  perhaps  even  for  a  year  before  death  there  was 
some  pain  upon  any  attempt  to  make  a  movement,  especially  of  the 
left  arm,  and  during  the  last  week  or  two  the  pain  on  movement  was 
intense  and  to  move  the  left  arm  caused  agony.  During  the  last  two 
or  three  weeks,  in  addition  to  the  weakness  of  both  the  legs  there  was 
partial  left  hemiplegia,  and  he  fell  into  a  stupor.  A  few  days  before 
death  he  expectorated  some  bloody  mucus.  The  respirations  became 
shorter  and  the  pulse  weak  and  irregular ;  finally  the  lungs  filled  up, 
and  he  died.  At  the  autopsy,  which  was  made  twenty  hours  after 
death,  the  spinal  cord  looked  a  little  small  and  was  somewhat  flabby, 
although  it  was  not  especially  easily  torn  or  crushed.  On  section  it 
was  seen  that  the  separation  of  the  gray  matter  from  the  white  was 
less  sharply  defined  than  is  natural,  and  the  gray  matter  seemed  to  be 
reduced  in  amount.  On  opening  the  thorax  and  abdomen  it  was  per- 
ceived that  there  was  an  enormous  accumulation  of  fat.  It  lay  in  the 
thorax,  in  the  pericardium,  and  upon  the  heart,  in  the  omentum,  and 
throughout  the  abdominal  cavity.  The  heart  presented  no  marked 
evidence  of  disease  except  the  very  thick  layer  of  fat  upon  its  surface 
and  slight  fibrous  thickening  of  the  aortic  leaflets.  The  lungs  at  their 
posterior  portions  were  almost  black,  and  here  and  there  non-crepi- 
tant,  but  the  greater  part  of  them  was  crepitant.  The  liver  presented 
no  gross  evidence  of  disease.  The  spleen  was  small  and  whitish,  and 


i9o  THE   ORIGIN   OF   DISEASE. 

the  capsule  a  little  thickened  and  wrinkled.  On  section  the  organ  ap- 
peared to  be  fibroid.  The  kidneys  were  of  only  half  the  natural  size, 
and  embedded  in  great  masses  of  fat,  which  were  nine  inches  in  the 
longer  by  five  in  the  shorter  diameter.  On  attempting  to  separate  the 
kidneys  from  the  fat  the  capsules  stripped  off,  remaining  with  the  fat, 
and  the  blood-vessels  which  pass  in  through  the  capsules  appeared 
to  be  both  numerous  and  enlarged.  The  surface  of  the  kidneys  was 
rough  and  granular,  and  on  section  it  was  seen  that  in  addition  to  their 
diminished  size  the  amount  of  the  cortical  substance  was  greatly  re- 
duced. The  muscles  of  the  body  and  limbs  were  shrunken  and  small, 
and  there  was  a  great  accumulation  of  fat.  Microscopical  examina- 
tion of  the  heart,  lungs,  liver,  spleen,  and  kidneys  revealed  the  exist- 
ence of  fibrosis  of  all  these  organs  and  extensive  vascular  disease.  If 
a  type  of  granular  kidney  were  sought  it  would  be  difficult  to  find  a 
more  perfect  one  than  was  exhibited  by  these  organs,  and  the  disease 
of  the  blood-vessels  was  so  marked  and  of  so  peculiar  a  type  that  one 
of  the  arterioles  has  been  used  for  illustration  (Fig.  14).  In  connec- 
tion with  the  picture  will  be  found  a  fuller  description  than  it  is  de- 
sirable to  introduce  here  under  the  head  of  diagnosis.  The  study  of 
the  cord  with  the  microscope  was  most  fruitful,  and  demonstrated  the 
presence  of  lesions  which  are  not  generally  described,  and  from  which 
important  deductions  both  in  regard  to  disease  in  general  and  to  diag- 
nosis in  particular  may  be  made.  A  number  of  the  illustrations  (Figs. 
134  to  137)  are  from  sections  of  this  cord,  and  these  are  described 
in  their  appropriate  places  in  connection  with  the  pictures. 

This  case  as  it  has  been  related  is  the  antithesis,  from  the  stand- 
point of  diagnosis,  of  that  which  has  been  given  (page  174)  as  typical 
of  Bright's  disease,  and  yet  the  post-mortem  lesions,  although  they 
varied  in  many  details,  were  so  much  alike  as  to  make  it  seem  that 
both  were  instances  of  the  same  disease.  Although  the  symptoms  of 
disease  of  the  spinal  cord  were  the  only  ones  that  ever  existed,  there 
was  something  in  the  condition  of  the  patient  which  made  me  feel 
assured  for  several  years  before  his  death  that  there  was  disease  of  the 
kidneys  and  of  the  heart  and  lungs.  It  is  most  important  for  the 
diagnostician  to  know  that  such  a  combination  of  conditions  as 
occurred  in  this  case  is  possible.  The  accepted  signs  of  disease  of  the 
kidneys,  although  sought,  were  always  absent,  even  the  specific  gravity 
of  the  urine,  which  is  said  to  be  low  in  contracted  kidney,  having  been, 
when  taken,  normal  or  above  the  normal,  and  yet  it  was  possible  to 
make  the  diagnostic  inference  that  the  kidneys  were  fibroid.  This 


DIAGNOSIS   IN   CHRONIC   DISEASE.  191 

was  done  simply  as  a  matter  of  general  principle,  of  deduction  from 
what  had  been  found  by  experience  in  other  similar  instances, — that 
in  a  man  with  such  marked  evidence  of  degenerative  disease  of  the 
spine,  the  process  having  lasted  through  years,  there  must  be  a 
generalized  fibrosis.  When  there  is  generalized  morbid  fibrosis  no 
organ  is  more  likely  to  suffer  than  the  kidney.  The  failure  of  the 
specific  gravity  to  fall  below  the  normal  is  a  most  important  point  in 
diagnosis,  for  it  is  taught  in  most  text-books,  and  very  generally  ac- 
cepted as  a  fact,  that  no  other  single  sign  is  so  unfailingly  present  in 
cases  of  contracted  kidney  as  low  specific  gravity  of  the  urine.  This 
has  long  seemed  to  me  to  be  an  inference  founded  upon  insufficient 
evidence.  Now  that  there  is  tangible  ground  for  it,  although  only 
one  case  in  point  is  offered,  it  is  time  to  assert  that  the  specific  gravity 
is  not  always  low  in  contracted  kidney,  and  that  other  and  better 
methods  of  establishing  the  diagnosis  must  be  sought.  This  means 
is  much  more  likely  to  be  found  in  a  careful  estimate  of  the  probable 
general  bodily  condition  and  deductions  therefrom  in  regard  to  dis- 
ease of  particular  organs  than  by  a  narrow  adherence  to  any  doctrine 
of  what  ought  to  be  the  specific  gravity  of  the  urine.  A  symptom 
which  was  mentioned  in  the  history,  and  which  is  worthy  of  further 
consideration,  is  that  there  was  pain  upon  motion  of  the  extremities  for 
some  time  before  death.  The  symptom  is  a  common  one  in  this  form 
of  disease  of  the  spine,  and  it  often  constitutes  a  striking  feature  during 
the  last  few  weeks  in  aged  persons  who  die  of  chronic  disease.  It 
must  be  the  result  of  inflammation  of  the  spine  or  its  meninges,  and 
it  presents  many  points  of  resemblance  to  the  general  hyperaesthesia 
which  is  one  of  the  ordinary  features  in  cases  of  acute  meningitis. 
Clinically  the  case  was  one  of  spinal  disease  pure  and  simple.  After 
all  methods  of  diagnosis  had  been  exhausted,  no  direct  evidence  of 
disease  other  than  that  of  the  spine  could  be  obtained.  Inference 
alone  led  to  the  conclusion  that  other  organs  were  involved,  and  the 
case  lends  support  to  the  view,  which  it  has  been  my  desire  to  make 
felt  at  every  point  throughout  this  work,  that  chronic  disease  is 
always  wide-spread  in  its  effects.  Although  clinically  a  case  of  spinal 
disease,  it  had  all  the  characteristics,  if  examined  from  the  side  of 
the  post-mortem  alone,  of  Bright's  disease.  This  aspect  of  the  case 
having  now  been  sufficiently  emphasized,  it  remains  to  ask  how  it 
should  be  regarded  as  concerns  its  classification  as  a  spinal  disease. 
What  diagnosis  should  have  been  made  after  consideration  of  the 
various  symptoms  and  from  the  results  of  physical  examination? 


192  THE   ORIGIN   OF   DISEASE. 

These  did  not  accord  with  any  of  the  descriptions  in  text-books  of 
the  various  forms  of  spinal  sclerosis  or  of  myelitis,  and  the  post- 
mortem examination  and  results  of  microscopical  study  as  shown  in 
the  illustrations  were  not  those  belonging  to  any  of  the  ordinary  classi- 
fied diseases.  It  might  be  well  to  give  a  new  name  to  this  form  of  dis- 
ease, the  spinal  fibrosis  and  degeneration  that  accompany  Bright's  dis- 
ease and  which  are  almost  parts  of  it.  So  far  as  concerns  the  lesions 
of  this  curious  degeneration,  it  is  not  necessary  to  describe  them  here, 
as  this  has  already  been  done  in  connection  with  the  illustrations. 
(Fig.  1 34  to  Fig.  1 37.)  The  diagnosis,  the  history,  and  the  symptoms 
of  the  case  have  already  been  detailed  in  full  (page  188).  It  has  been 
my  lot  to  meet  with  this  condition  of  the  spinal  cord  a  number  of 
times,  but  only  in  one  other  instance  have  I  met  with  it  in  a  form 
parallel  with  that  of  the  case  which  has  been  given  in  full,  in  which 
the  spinal  symptoms  were  the  only  ones  manifest  during  life,  and  yet 
the  lesions  of  extensive  generalized  disease  were  found  at  the  post- 
mortem examination.  In  that  case  there  was  strong  reason  to  believe 
that  syphilis  was  the  underlying  cause.  In  other  cases  the  same 
symptoms  of  spinal  disease,  the  curious  dragging  of  the  feet,  uncer- 
tainty of  equilibrium,  and  finally  incomplete  paraplegia  of  the  legs, 
appeared  as  complications  in  persons  suffering  with  the  ordinary  con- 
ditions observed  in  Bright's  disease.  The  disease  is  one  in  which  the 
lesions  occupy  all  parts  of  the  spinal  cord,  and  are  not  confined  to 
particular  regions  as  in  the  spinal  diseases  usually  described,  and 
the  symptoms  do  not  conform  with  any  of  the  ordinary  types. 

In  practice  it  is  not  rare  to  meet  with  cases  of  illness  in  which 
there  is  prostration  and  even  fever  and  yet  no  satisfactory  reason  for 
the  attack  can  be  discovered.  It  has  happened  to  most  clinicians, 
probably,  to  have  this  experience.  Such  an  attack  may  last  for  many 
weeks  or  even  longer,  and  after  it  is  over  no  explanation  be  forth- 
coming. Without  doubt  there  is  always  a  cause,  and  it  is  probable 
that  processes  are  taking  place  somewhere  in  the  body  resulting  in 
the  production  of  lesions  that  would  be  visible  to  the  unaided  eye  or 
could  be  seen  with  the  microscope  if  it  were  known  where  to  look 
for  them.  It  has  happened  to  me  again  and  again  to  see  such  attacks 
of  sickness,  and  my  mind  has  been  forced  to  the  conclusion  that  they 
must  often  be  the  occasion  of  organic  lesions.  It  has  been  stated  a 
number  of  times  in  the  chapters  dealing  with  the  various  organs  that 
lesions  which  were  quite  unanticipated  are  often  found.  It  is  a  fair 
diagnostic  conclusion  in  these  vague  cases,  especially  when  they  are 


DIAGNOSIS   IN   CHRONIC   DISEASE.  193 

of  any  great  degree  of  severity,  that  some  inflammatory  or  degenera- 
tive process  is  taking  place  and  will  result  in  organic  lesion. 

That  mistakes  in  diagnosis  are  made  no  one  will  deny,  and  some- 
times the  symptoms  are  so  misleading  that  they  cannot  be  avoided. 
One  disease  so  closely  imitates  another  that  it  is  impossible  to  avoid 
being  misled.  It  has  been  pointed  out  how  wide-spread  chronic  dis- 
ease is  in  the  effects  it  produces,  and  it  is  certain  that  chronic  pro- 
cesses usually  latent  in  their  mode  of  progress  are  liable  to  occasion 
acute  and  even  violent  outbreaks  in  one  part  or  another.  It  is  impor- 
tant for  the  clinician  to  keep  this  fact  in  mind,  for  the  symptoms  of 
some  one  of  the  acute  diseases  may  be  so  closely  imitated  as  to  give 
rise  to  a  mistake  in  diagnosis.  This  recalls  a  case  of  perihepatic 
abscess  the  outcome  of  long-standing  chronic  disease  which  was  mis- 
taken for -typhoid  fever.  The  liver  from  this  patient  has  been  used  to 
illustrate  certain  peculiarities  of  disease  of  that  organ  (Figs.  76  and 
77),  of  which  a  description  will  be  found  in  connection  with  the  pic- 
tures. The  man  was  sick  for  several  weeks  with  what  seemed  more 
like  typhoid  fever  than  anything  else ;  at  any  rate,  no  other  diagnosis 
could  be  made,  and  it  was  only  the  post-mortem  examination  that  re- 
vealed the  presence  of  a  large  perihepatic  abscess  and  chronic  lesions 
that  must  have  existed  a  long  time  before  the  abscess  which  was  the 
immediate  cause  of  death.  The  fact  is  interesting  that  these  wide- 
spread chronic  lesions  may  give  rise  to  acute  inflammatory  out- 
breaks, and  it  is  very  important,  from  the  diagnostic  point  of  view,  to 
remember  that  such  a  thing  is  possible.  Mistakes  may  be  made  even 
in  a  disease  of  such  definite  nature  as  typhoid  fever  is  commonly 
thought  to  be.  It  has  already  been  pointed  out  that  there  is  some 
reason  for  believing  typhoid  fever  to  be  a  less  definite  entity  than  it 
is  generally  considered,  and  that  nature  does  not  draw  abrupt  lines 
separating  one  disease  from  another  to  such  an  extent  as  is  usually 
believed. 

A  singular  fact,  and  one  worthy  of  consideration,  is  that  a  sudden 
violent  diarrhoea  or  cholera  morbus  in  an  elderly  individual  not 
usually  subject  to  such  attacks  is  generally  an  indication  of  the 
existence  of  organic  disease.  Such  organic  disease  often  has  been 
entirely  latent,  and  the  first  intimation  of  its  existence  is  the  unex- 
pected attack  of  intestinal  disorder.  So  often  has  an  experience  of 
this  kind  come  under  my  notice  that  it  is  not  putting  the  matter  too 
strongly  to  say  that  a  sudden  intestinal  attack  in  an  elderly  person 
not  previously  subject  to  such  attacks  should  always  be  considered  a 

'3 


194  THE   ORIGIN   OF   DISEASE. 

reason  for  setting  in  motion  every  diagnostic  method  of  search  for  or- 
ganic disease.  If  nothing  is  found,  it  is  a  safe  inference  that  such  dis- 
ease exists  if  the  attack  was  violent  and  if  there  is  no  other  reason  to 
explain  it.  It  is  not  rare  that  an  acute  attack  of  diarrhoea  or  of  cholera 
morbus  gives  the  first  intimation  of  the  existence  of  grave  organic 
disease  of  the  heart  or  of  Bright's  disease.  The  cause  of  this  con- 
nection between  acute  intestinal  attacks  and  serious  disease  of  the 
organs  cannot  now  be  explained,  but  the  lack  of  an  understanding 
of  it  is  no  reason  why  the  connection  should  not  be  kept  in  mind  and 
utilized  in  diagnosis. 

If  an  acute  intestinal  attack  in  a  person  not  subject  to  such  attacks 
should  be  considered  as  a  warning  of  the  existence  of  some  disease, 
the  occurrence  of  epistaxis  in  an  elderly  person  not  subject  to  nose- 
bleed should  be  regarded  by  the  diagnostician  with  even  more  sus- 
picion. It  is  an  almost  infallible  sign  of  organic  disease.  There  is 
no  occasion  at  present  to  discuss  extensively  this  curious  fact,  which 
cannot  now  be  completely  explained.  Although  nose-bleed  occurring 
after  middle  life  is  frequently  a  sign  of  organic  disease,  it  is  not  in- 
tended to  say  that  it  is  impossible  for  uncomplicated  epistaxis  to 
occur,  but  simply  that  in  practice  when  an  elderly  person  not  consti- 
tutionally subject  to  it  has  nose-bleed,  especially  if  it  be  severe,  it  will 
almost  always  be  found  that  there  is  organic  disease.  The  diseases 
most  commonly  found  under  the  circumstances  are  kidney  disease  and 
organic  heart  disease,  but  in  my  experience  the  latter  is  less  common. 
The  association  of  epistaxis  and  heart  disease  is  an  old  and  well- 
known  clinical  phenomenon.  It  must  be  that  such  nose-bleed  is  due 
to  organic  change  of  the  walls  of  the  supply-vessels,  for  it  is  not  con- 
ceivable that  healthy  vessels  would  rupture  without  cause.  That  dis- 
ease of  other  organs  should  be  brought  to  light  in  this  way  is  another 
proof  of  the  wide-spread  nature  of  the  lesions  of  chronic  disease,  but 
the  diagnostic  point  to  be  recollected  and  to  be  here  emphasized  is 
that  when  such  epistaxis  as  has  been  described  occurs,  the  diagnosis 
of  organic  disease  may  generally  be  made.  The  form  that  will  be 
most  frequently  found  is  disease  of  the  kidney.  It  would  be  difficult 
to  exaggerate  the  importance  of  this  diagnostic  inference,  and  it  may 
be  added  that  if  thorough  examination  of  an  elderly  person  who  has 
had  severe  epistaxis  fails  to  lead  to  the  detection  of  any  disease,  its 
existence  should  still  be  suspected  until  a  sufficient  time  has  elapsed 
to  make  it  reasonable  to  suppose  that  good  health  is  still  maintained. 

A  common  symptom  in  elderly  persons  is  confusion   of  speech 


DIAGNOSIS   IN   CHRONIC   DISEASE.  195 

with  slight  paralysis  or  paralytic  weakness,  rapidly  passing  away  and 
leaving  the  individual  just  as  he  was  before.  Such  attacks  most  fre- 
quently occur  in  persons  past  middle  life,  and  study  of  their  history 
generally  brings  to  light  that  there  had  been  some  previous  failure  of 
health.  Although  this  is  not  invariably  the  case,  it  is  so  in  the  great 
majority  of  instances.  The  question,  What  is  the  precise  cause  of 
such  symptoms  ?  is  one  which  it  is  very  desirable  to  answer.  That, 
however,  which  it  is  most  necessary  to  explain  in  a  discussion  of  diag- 
nosis is  what  should  be  inferred  when  a  case  of  the  kind  is  met  with 
in  practice.  It  is  impossible  at  present  to  say  with  certainty  what 
causes  such  attacks,  but  it  seems  hardly  likely  they  can  be  due  to 
apoplexy.  It  is  difficult  to  believe  that  paralysis  or  confusion  of 
speech  caused  by  the  rupture  of  a  vessel  and  effusion  of  blood, 
which  necessarily  destroys  some  portion  of  the  brain-substance,  could 
pass  away  so  rapidly  as  these  attacks  do.  It  has  happened  to  me 
many  times  to  see  persons  with  slight  facial  palsy  and  difficulty  of 
speech  or  confusion  of  mind  which  disappeared  entirely  after  two  or 
three  hours.  In  most  cases  there  have  been  a  number  of  attacks  in 
the  course  of  two  or  three  years.  Sometimes  an  attack  may  take 
the  form  of  difficulty  in  walking,  or  there  may  be  confusion  of  mind 
or  difficulty  of  expression  in  speech  alone.  Patients  affected  in  this 
way  invariably  have  failing  health,  and  the  end  may  be  in  an  attack  of 
apoplexy  or  Bright's  disease  or  pneumonia  or  any  other  of  the  dis- 
eases to  which  elderly  people  are  prone.  As  already  said,  it  seems 
rather  a  far-fetched  explanation  to  attribute  the  attacks  to  hemorrhage 
into  the  brain,  and  certainly  there  have  been  no  post-mortem  obser- 
vations to  support  such  a  view.  Clots  are  so  often  found  in  the  blood- 
vessels in  many  parts  of  the  system,  and  they  are  so  commonly  found 
in  vessels  of  the  smallest  size,  that  experience  has  made  me  believe 
that  clots  in  unruptured  vessels  are  the  cause  of  much  more  disease 
than  is  commonly  known,  and  that  they  are  often  formed  and  after- 
ward rapidly  removed,  leaving  the  vessel  in  a  condition  nearly  natural. 
Such  a  theory  if  it  could  be  sustained  would  explain  the  passing  cere- 
bral attacks  which  have  been  described.  However  this  may  be,  it  is 
certain  that  such  an  attack  has  an  important  diagnostic  significance.  It 
is  a  sign  that  may  be  relied  upon  of  the  existence  of  vascular  disease, 
and  that  the  vascular  disease,  as  is  its  habit,  is  of  wide-spread  extent. 
In  addition  to  changes  in  the  blood-vessels  which  are  inevitable  to 
age,  the  diagnosis  may  safely  be  made  of  grave  organic  disease,  and  if 
no  certain  signs  of  it  can  at  once  be  found,  they  will  appear  within  a 


196  THE   ORIGIN   OF   DISEASE. 

year  or  two  if  the  degenerative  processes  that  have  begun  continue  at 
their  ordinary  rate.  Whether  the  disease  which  first  manifested  itself 
in  the  brain  will  continue  its  work  there,  or  will  break  out  in  the 
heart,  lungs,  kidneys,  or  elsewhere,  cannot  be  known  if  the  examina- 
tion of  those  organs  fails  to  reveal  the  signs  of  disease.  The  diag- 
nosis, however,  of  organic  disease  may  safely  be  made,  and  time  will 
show  what  form  it  is  to  take. 

Recently  much  has  been  written  of  an  unnatural  increase  of  the 
intravascular  blood-pressure.  It  is  commonly  spoken  of  as  a  clinical 
symptom  of  great  importance,  and  as  if  it  were  an  easy  matter  to 
ascertain  its  existence.  This,  however,  is  far  from  being  the  case. 
There  can  be  no  doubt  that  the  heart,  by  the  changing  force  of  its 
action,  can  vary  the  degree  of  pressure  within  the  arteries,  and  it  is 
probable  that  other  conditions  also  contribute  to  the  same  end ;  but 
it  is  equally  certain  that  for  the  diagnostician  nothing  but  the  intro- 
duction of  an  instrument  of  precision  into  the  blood-stream,  as  has 
been  so  often  done  in  the  lower  animals,  can  give  final  information 
upon  the  point.  It  would  not  be  desirable  to  attempt  here  to  discuss 
in  full  this  most  intricate  subject,  but  it  may  be  said  that  many  of  the 
untenable  theories  which  pass  current  lead  to  most  unfortunate  errors 
in  diagnosis,  and  thus  to  wrong  treatment,  which  is  still  worse.  In 
the  chapter  on  the  blood-vessels  it  has  been  pointed  out  that  the  dis- 
ease to  which  they  are  most  liable  is  fibroid  thickening  of  their  walls, 
and  every  one  knows  how  common  enlargement  of  the  heart  is.  It  is 
when  the  heart  is  of  increased  size  that  the  pulse  most  often  has  the 
character  usually  called  "  high  tension."  There  are  at  least  two  rea- 
sons for  thinking  the  so-called  high  tension  character  is  often  present 
when  probably  the  blood-pressure  is  below  instead  of  above  the  nor- 
mal. The  first  of  these  is  that  the  force  with  which  an  enlarged  heart 
beats  is  often  much  less  than  the  normal,  and  the  second  that  arterial 
disease  is  often  of  such  a  character  as  to  change  the  walls  of  the  ves- 
sel so  as  to  give  the  impression  of  a  high  tension  pulse  when  in  fact 
the  blood-pressure  is  low.  When  the  walls  of  an  artery  become  thick 
it  is  impossible  by  feeling  its  pulsations  to  ascertain  whether  the  pecu- 
liar sensation  of  hardness  which  is  conveyed  to  the  finger  is  due  to 
stiffness  of  the  walls  or  to  an  unnatural  hardness  of  the  column  of 
blood  that  is  flowing  within  it.  The  correctness  of  this  statement  may 
be  verified  by  any  one  who  will  take  the  trouble  to  study  during  life  the 
condition  of  the  radial  and  femoral  or  other  arteries  that  lie  beneath 
the  skin,  and,  having  found  vessels  with  the  high  tension  character, 


DIAGNOSIS   IN   CHRONIC   DISEASE.  197 

examine  them,  as  the  opportunity  offers,  post  mortem.  Extensive 
study  carried  out  along  the  lines  indicated  has  led  me  to  conclude  that 
the  so-called  pulse  of  high  tension  is  unreliable  as  a  diagnostic  indica- 
tion, and  that  it  is  probable  that  when  it  is  present  the  blood-pressure 
is  often  low,  this  misleading  result  being  brought  about  by  fibroid 
thickening  of  the  arterial  walls.  In  the  chapter  on  blood-vessels  it  was 
shown  that  the  radial  artery,  which  is  the  one  from  which  the  charac- 
ter of  the  pulse  is  most  often  judged,  is  peculiarly  liable  to  become 
thick-walled.  It  is  not  necessary  to  dilate  fully  upon  the  misleading 
results  obtained  by  feeling  the  heaving  beat  of  an  enlarged  heart.  The 
conclusion  that  such  an  organ  pumps  with  unnatural  force  is  often  a 
wrong  one,  for  the  great  impression  produced  upon  the  hand  placed 
over  such  a  heart  may  be  due  simply  to  the  increased  size  of  the  organ 
and  to  its  being  too  large  for  the  space  that  contains  it.  It  has  been 
shown  in  the  chapter  on  the  heart  that  in  cases  of  hypertrophy  the  walls 
are  in  most  instances  degenerated  and  probably  weak  instead  of  having 
increased  strength.  For  the  reasons,  therefore,  that  an  enlarged  heart 
with  a  heaving  impulse  often  is  a  very  feeble  pump,  and  that  thick- 
walled  arteries  give  an  impression  identical  with  that  produced  by 
increased  intravascular  pressure,  the  so-called  high  tension  pulse  is 
very  unreliable  as  a  diagnostic  sign,  and  is  often  present  when  the 
circulation  is  feeble  and  inefficient  rather  than  bounding  and  danger- 
ously strong. 

A  most  difficult  question  in  diagnosis  and  one  impossible  at  present 
to  answer  conclusively  is,  What  is  the  relation  of  gout  to  Bright's 
disease?  Although  complete  knowledge  is  as  yet  not  even  to  be 
hoped  for,  the  subject  is  so  important,  and  in  practice  the  two  dis- 
eases, which  in  their  typical  forms  of  development  are  so  utterly  un- 
like, are  so  often  found  together,  that  the  discussion  of  their  relation- 
ship should  not  be  avoided.  There  is  no  difficulty  in  recognizing 
gout  in  its  typical  form  when  it  attacks  the  joints,  and  it  is  hardly 
necessary  to  say  that  Bright's  disease  when  fully  developed  consti- 
tutes a  very  distinct  clinical  picture.  The  difficulty  is  encountered 
when  one  comes  to  deal  with  what  are  called  "  gouty  tendencies,"  and 
sometimes  to  decide  why  gouty  heart  and  gouty  kidney  are  so  named. 
The  names  were  introduced  to  describe  attacks  of  illness  encountered 
in  practice,  and  their  very  existence  is  an  indication  of  the  relation- 
ship of  gout  and  Bright's  disease.  There  are  cases  with  symptoms 
so  vague  that  no  particular  organ  or  part  can  be  connected  with 
the  attack,  and  yet  something  suggests  gout  so  strongly  that  it  has 


198  THE   ORIGIN   OF   DISEASE. 

become  the  custom  to  speak  of  a  "  gouty  tendency,"  though  it  may 
be  impossible  to  say  precisely  why  this  is.  On  the  other  hand,  local 
disease  may  appear  in  an  unusual  form  and  may  last  so  long  as  to 
make  it  appear  that  there  must  be  some  constitutional  fault  to  cause 
it :  such  attacks  are  said  to  be  of  "  gouty  origin."  As  an  instance  of 
the  latter  form  of  disease,  a  man  or  woman  of  fifty  may  have  pain  in 
the  foot  lasting  for  months  or  even  longer  and  with  only  slight  ex- 
ternal evidence  of  disease.  Such  an  attack  may  come  after  a  trifling 
local  injury,  or  there  may  have  been  no  accident  to  account  for  it. 
There  may  be  slight  swelling  or  redness,  or,  again,  no  external  evidence 
of  inflammation.  Very  severe  pain  is  complained  of,  and  there  can  be 
no  doubt  that  this  is  real,  for  persons  so  affected  will  refuse  to  use  the 
affected  foot  at  all,  and  remain  bedridden  or  seated  in  a  chair.  Such 
disease  is  said  to  be  based  upon  a  gouty  constitutional  fault.  Is  it  not 
more  like  Bright's  disease  local  in  the  foot?  The  resemblance  of  the 
gouty  constitutional  taint  to  Bright's  disease  is  very  close.  Much  has 
been  written,  especially  in  Great  Britain,  of  the  gouty  heart  and  of  the 
gouty  kidney.  What  are  they  but  the  heart  and  kidney  of  Bright's 
disease  ?  It  is  the  old,  or  the  prematurely  old,  or  the  dissipated,  who 
are  so  affected.  After  all,  it  is  but  old  age  or  age  in  youth,  the  com- 
bination of  fibroid  growth  with  the  process  of  inflammation,  and  all 
the  infinitely  various  clinical  forms  are  produced  according  to  the  re- 
spective quantities  of  the  two  ingredients — morbid  fibrosis  and  inflam- 
mation— in  the  mixture.  The  practical  lesson  to  be  learned  is  that 
pathology  has  outrun  diagnosis,  so  that  the  knowledge  is  forced  upon 
us  that  diseases  that  have  been  considered  to  be  distinct  are  related. 
It  must  be,  too,  that  vascular  disease,  fibrosis,  and  the  inflammations 
that  are  sure  to  follow  in  their  wake  have  much  to  do  with,  if  they 
are  not  the  causes  of,  both  gout  and  Bright's  disease. 

In  the  diagnosis  of  chronic  disease  it  must  be  remembered  that  the 
beginnings  are,  in  the  nature  of  things,  obscure.  Many  of  the  patho- 
logical lesions  which  are  illustrated  in  the  chapters  on  the  various 
organs  have  their  origin,  and  even  attain  considerable  proportions, 
without  manifesting  their  existence  by  any  external  sign.  Another 
mode  for  their  production  is  through  vague  attacks  of  illness  which 
are  difficult  to  classify.  Such  attacks  have  already  been  discussed  in 
this  chapter.  It  has  been  shown  that  the  latent  existence  of  these 
lesions  is  of  very  great  importance  to  the  individual,  as  in  time  they 
accumulate  until  in  themselves  they  constitute  grave  chronic  disease, 
or  else  if  the  person  is  seized  by  acute  illness  they  have  so  lamed  the 


DIAGNOSIS   IN   CHRONIC   DISEASE.  199 

organism  that  they  have  a  preponderating  influence  in  determining  a 
fatal  ending  of  an  attack  that  would  not  have  killed  a  sound  person. 
For  the  diagnostician  nothing  can  be  more  important  than  to  recog- 
nize chronic  disease  in  its  very  origin.  This  can  be  done  only  by  re- 
membering that  it  is  almost  always  wide-spread  in  its  effects,  and  by 
the  observation  of  very  little  things.  There  are  no  set  symptoms,  and 
it  is  largely  by  inference  that  a  correct  estimate  can  be  made.  Per- 
haps no  one  thing  is  more  important  for  the  diagnostician  to  know 
than  that  vascular  disease  and  fibrosis  are  certain  to  come  in  all  men 
if  they  live  to  be  old  enough.  The  corollary  is  that  a  similar  state  is 
produced  earlier  if  the  necessary  conditions  exist,  and  thus  chronic 
disease  resembles  old  age  in  youth. 


CHAPTER   XIV. 

PROGNOSIS    IN    CHRONIC    DISEASE. 

PROGNOSIS  will  be  dealt  with  like  the  various  subjects  heretofore 
treated.  No  attempt  will  be  made  to  discuss  it  in  full,  but  only  a 
record  made  of  such  experiences  as  may  aid  to  extend  our  power  to 
forecast  the  future  in  disease  and  to  correct  errors.  In  chronic  disease 
the  prognosis  is  often  much  more  gloomy  than  the  occasion  warrants, 
because  when  the  conclusion  has  been  reached  that  a  case  is  incurable 
it  is  forgotten  that  it  is  not  the  question  of  its  curability  or  incurability 
alone  that  should  govern  the  forecast  of  the  future.  The  fact  that 
the  patient  is  alive  at  the  moment  of  examination  establishes  that  his 
immediate  state  of  disease  is  compatible  with  the  continuance  of  life : 
the  real  question  for  prognosis  is  the  rate  of  progress.  In  practice 
this  most  important  consideration  is  commonly  forgotten,  and  so  soon 
as  the  diagnosis  of  incurable  disease  is  made  it  is  concluded  that 
death  is  imminent.  In  a  disease  like  cancer  this  conclusion  is  reason- 
able enough,  for  it  is  of  comparatively  rapid  progress,  and  under  all 
ordinary  circumstances  a  few  years  put  a  period -to  the  life  of  the 
individual  attacked  by  it.  The  question,  however,  is  very  differ- 
ent in  ordinary  chronic  disease:  it  has  no  fixed  habit  in  its  rate 
of  progress.  An  individual  suffering  with  chronic  incurable  disease 
may  live  indefinitely  if  the  disease  ceases  to  progress.  Nothing  prob- 
ably could  better  illustrate  this  than  what  sometimes  takes  place 
with  cataract,  which  may  cease  to  grow,  the  person  never  becoming 
blind.  Many  unfortunate  errors  in  prognosis  have  been  made,  inevi- 
table blindness  having  been  prophesied  of  persons  with  cataract  who 
never  became  blind.  Such  errors  are  less  common  than  formerly, 
because  the  specialists  have  learned  that  it  is  impossible  for  them 
to  forecast  the  rate  of  progress,  and  that  there  may  even  be  no 
progress.  The  parallel  between  fibroid  disease  and  cataract  may  be 
carried  further,  for  traumatic  cataract  may  occur  in  early  life.  In  that 
form  it  seems  like  age  in  youth  as  much  as  many  of  the  chronic  dis- 
eases which  belong  naturally  to  age  but  can  under  favoring  circum- 
stances be  produced  in  youth.  It  has  for  a  good  while  been  understood 
that  acute  disease  of  the  kidney  frequently  ends  in  complete  recovery, 

200 


PROGNOSIS   IN   CHRONIC   DISEASE.  201 

but  chronic  kidney  disease  is  still  generally  considered  to  warrant  a 
very  grave  prognosis,  in  most  instances  even  that  death  will  soon 
ensue.  Chronic  Bright's  disease  is  considered  both  incurable  and 
rapidly  fatal.  A  few  years  ago  skilled  microscopists  were  willing  to 
undertake  to  make  a  prognosis  from  an  examination  of  the  urine  alone 
without  having  seen  the  patient  and  with  no  knowledge  of  his  con- 
dition. If  oily  casts  were  found,  it  was  announced  that  death  would 
ensue  within  two  years.  The  erroneousness  of  such  a  position  is  now 
thoroughly  recognized,  but  even  yet  it  is  not  so  well  known  as  it 
should  be  how  long  men  who  have  had  chronic  Bright's  disease  live 
and  even  enjoy  good  health.  The  presence  of  albumen  and  casts 
in  the  urine  continuously  for  any  considerable  time  is  a  positive  sign 
of  disease  of  the  kidney,  but  only  a  study  to  ascertain  the  state  of 
the  other  organs  and  of  the  general  condition  can  yield  information 
sufficient  to  warrant  a  prognosis.  On  the  other  hand,  it  has  been 
shown  (page  190)  that  the  most  extensive  disease  of  the  kidneys  may 
exist  and  fail  to  reveal  itself  by  anything  in  the  urine.  To  illustrate, 
two  cases  may  be  mentioned  of  men  who  were  ill  when  about  sixty 
years  of  age.  In  both  instances  there  were  albumen  and  casts  in 
the  urine  during  about  two  years.  One  of  them  had  catarrhal  pneu- 
monia, and  the  other  bronchitis  and  coryza.  Both  recovered  and 
enjoyed  good  health  afterward,  one  dying  seventeen  years  later,  and 
the  other  is  still  alive  after  twenty-one  years,  and  is  now  more  active 
than  the  generality  of  men  of  eighty.  There  can  be  little  doubt  that 
the  kidneys  were  left  scarred  and  injured  by  the  disease  so  many  years 
ago,  and  it  is  probable  that  in  men  so  old  this  made  constant  latent 
progress,  but  the  lesson  taught  is  that  a  very  grave  prognosis  is  not 
warranted  under  such  circumstances,  for  although  the  disease  may 
have  been  and  probably  was  incurable,  its  existence  was  not  incom- 
patible with  the  subsequent  possession  of  good  health.  It  is  not  rare 
to  see  attacks  of  jaundice  in  elderly  persons  accompanied  with  such 
symptoms  as  seem  to  indicate  grave  disease  of  the  liver  and  at  the 
same  time  the  signs  of  general  fibroid  and  vascular  disease.  Such 
attacks  not  rarely  end  in  recovery.  Under  the  circumstances  there  is 
probably  severe  inflammation  of  a  part  or  the  whole  of  a  liver  already 
lamed  by  fibroid  and  vascular  change,  and  it  is  almost  certain  that  the 
organ  is  left  in  worse  condition  than  before  the  attack.  The  prog- 
nosis, however,  should  not  be  too  grave,  for  even  if  the  patient  has 
incurable  disease  this  will  be  of  comparatively  little  importance  if  it 
remains  latent,  so  that  he  can  continue  to  enjoy  comfortable  health. 


202  THE   ORIGIN   OF   DISEASE. 

Few  symptoms  are  more  alarming  and  at  first  sight  seem  more  posi- 
tively to  warrant  a  bad  prognosis  than  excessive  irregularity  of  the 
action  of  the  heart.  Great  irregularity  of  the  cardiac  action  when  it 
lasts  for  a  length  of  time  is  to  be  looked  upon  as  an  indication  of 
organic  disease.  In  elderly  persons  it  is  probably  a  sign  of  the  exist- 
ence of  some  of  the  degenerative  changes  described  in  the  chapter  on 
the  heart.  To  make  a  correct  prognosis  in  such  a  case  it  is  necessary 
to  recollect  that  the  future  depends  upon  the  progress  of  the  disease, 
for  the  fact  that  the  patient  continues  to  live  shows  that  it  must  in- 
crease to  cause  death.  The  irregularity  of  the  heart  which  it  is  in- 
tended to  indicate  is  not  the  mere  intermitting  which  is  very  common 
at  almost  all  periods  of  life,  but  irregularity  to  such  a  degree  that  no 
three  pulsations  of  the  organ  follow  one  another  in  regular  and  even 
succession  of  time  and  force.  This  violent  irregularity  may  be  present 
for  as  much  as  ten  years  and  the  patient  still  be  living  a  comfortable 
and  active  life  at  seventy-nine  years. 

Having  described  symptoms  and  forms  of  organic  disease  the  ex- 
istence of  which  is  not  incompatible  with  the  continuance  of  enjoyable 
health,  it  will  be  well  to  try  to  show  something  of  the  other  side,  and 
to  indicate  under  what  conditions  it  is  likely  that  life  cannot  be  greatly 
prolonged.  This  will  not  be  easy  to  accomplish,  but  a  few  things  can 
be  mentioned  that  may  generally  be  considered  to  warrant  the  prog- 
nosis of  speedy  death.  It  has  been  shown  that  for  practical  purposes 
it  is  correct  to  say  that  the  direct  cause  of  death  is  always  to  be  found 
in  the  brain,  the  heart,  or  the  lungs.  It  will  be  unnecessary  here  to 
say  very  much  of  prognosis  in  brain  disease.  Although  there  is  the 
best  reason,  derived  from  the  study  of  pathology,  for  thinking  that 
the  brain  often  partakes  in  a  most  important  way  in  the  wide-spread 
processes  of  chronic  disease,  the  involvement  of  the  brain  does  not 
generally  occupy  the  attention  very  much.  The  reason  is  that  if  there 
are  symptoms  which  distinctly  denote  organic  brain  lesion  the  disease 
is  judged  and  the  prognosis  made  according  to  such  rules  as  exist  for 
prognosis  in  brain  disease.  On  the  other  hand,  if  the  brain  is  in- 
volved in  a  latent  manner  as  a  complication  of  general  chronic  disease 
and  death  takes  place  owing  to  the  brain  directly,  it  is  generally  so 
sudden  that  there  is  no  prognosis.  Sudden  death  in  most  instances  is 
unexpected  death,  and  therefore  means  a  total  failure  of  prognosis.  It 
is  not  intended  to  say  that  in  the  latter  stages  of  chronic  disease  no 
attention  should  be  paid  to  the  bodily  feebleness  and  the  clouding  of 
the  intellect  as  indications  of  the  approach  of  death,  but  that  in  most 


PROGNOSIS   IN   CHRONIC   DISEASE.  203 

instances  they  cannot  be  made  use  of  to  forecast  the  future  as  can  be 
done  by  other  means,  for  they  generally  come  only  toward  the  last, 
when  it  is  evident  that  death  is  near.  From  the  examination  of  the 
heart  and  lungs  can  be  derived  the  most  certain  knowledge  that 
chronic  disease  has  reached  the  stage  when  the  prognosis  of  speedy 
death  should  be  made.  It  has  been  shown  that  prognosis  based  upon 
an  estimate  of  the  state  of  the  kidney  is  very  unreliable,  because  the 
most  extreme  degrees  of  fibrosis  and  contraction  may  exist  and  com- 
fortable health  be  maintained.  Although  it  is  certain  that  inflamma- 
tion of  the  kidneys  may  induce  death,  there  is  as  yet  so  little  definite 
knowledge  obtainable  in  regard  to  their  inflammation  during  life  that 
little  can  be  learned  in  that  way.  It  is  true,  therefore,  but  the  fact  is 
not  given  its  due  weight  in  practice,  that  prognosis,  even  when  the 
case  is  plainly  one  of  chronic  Bright's  disease,  should  be  based  much 
more  upon  a  study  of  the  condition  of  the  heart  and  lungs  than  upon 
anything  else.  It  has  been  repeatedly  stated  that  chronic  organic  dis- 
ease is  usually  wide-spread,  and  therefore  in  prognosis  each  of  the 
organs  should  be  thought  of  in  turn  and  an  effort  made  to  form  an 
estimate  of  their  probable  condition,  but  no  other  organs  so  lend 
themselves  to  physical  diagnosis  as  do  the  heart  and  lungs,  which 
throughout  life  are  perpetually  in  motion  and  always  making  sounds, 
while  the  workings  of  all  the  other  organs  are  silent.  The  worst  may 
be  mentioned  first.  There  is  no  chronic  disease  which  warrants  a 
more  gloomy  prognosis  than  that  in  which  the  heart  has  become 
very  large,  with  a  heaving  impulse,  perceptible  over  an  unnaturally 
great  area,  and  the  lungs  begin  to  show  signs  of  inflammation.  Cor- 
rect observation  of  the  condition  of  the  heart  and  lungs  and  a  just 
interpretation  of  the  meaning  of  the  signs  yielded  by  their  examina- 
tion has  long  seemed  to  me  to  constitute  the  key  to  success  in  prog- 
nosis in  chronic  disease.  It  is  not  that  the  other  organs — the  liver, 
the  kidneys,  the  digestive  apparatus,  and  even  the  spleen — may  not 
have  a  preponderating  influence  in  causing  death,  but  they  are  deeply 
hidden  and  work  silently  and  their  condition  cannot  be  known,  and 
finally  they  must  work  through  the  heart  and  lungs,  and  by  the  effect 
that  is  produced  upon  them  the  fatal  result  is  brought  about.  It  is 
difficult  to  know  to  what  extent  to  dilate  upon  this  subject,  for  there 
is  so  much  that  can  be  acquired  only  by  experience,  and  many  of  the 
signs  that  indicate  that  disease  is  drawing  to  its  end  are  so  subtile 
that  they  can  hardly  be  put  in  words.  The  fact  that  in  the  great 
majority  of  instances  the  direct  cause  of  death  is  to  be  found  in  the 


204  THE   ORIGIN   OF   DISEASE. 

lungs  has  already  been  discussed  (page  96),  and  it  follows  that  it  is 
most  important  in  prognosis  to  attain  as  just  an  estimate  as  possible 
of  their  condition.  It  has  also  (Chapter  VI.)  been  shown  that  the 
lungs  are  involved  as  often  as  or  more  often  than  the  other  organs  in 
the  fibroid  processes  which  are  common  to  the  advance  of  life  and  to 
chronic  disease.  When  in  addition  to  these  chronic  lesions,  which 
may  be  inferred  in  most  instances  to  exist,  even  if  the  direct  evi- 
dences of  their  presence  are  absent,  there  comes  oedema  of  the  lungs 
or  hypostatic  congestion  or  hypostatic  pneumonia,  the  condition  of  the 
patient  is  bad,  and  if  he  does  not  succumb  to  the  immediate  attack  he 
will  to  a  subsequent  one.  The  certainty  of  the  recurrence  of  these 
attacks  is  surprising,  and  sooner  or  later  one  of  them  must  prove 
fatal.  The  mode  of  livelihood  is  a  most  important  consideration  in 
prognosis  in  chronic  disease,  especially  if  it  has  been  ascertained  that 
the  heart  and  lungs  have  become  organically  diseased.  The  fatality 
among  the  poorer  classes,  who  must  earn  their  livelihood  by  physical 
labor,  which  necessarily  carries  with  it  exposure,  is  exceedingly  great, 
while,  on  the  other  hand,  it  is  wonderful  how  life  is  prolonged  among 
those  who  are  surrounded  by  every  care  and  who  will  take  advice  to 
avoid  effort  and  exposure.  The  taking  of  cold  and  physical  effort 
soon  cause  a  recurrence  of  inflammatory  disease  in  persons  suffering 
with  chronic  lesions  who  might  otherwise  have  escaped  for  a  long 
period. 

The  principal  purpose  of  this  chapter  is  to  emphasize  two  points : 
first,  that  it  is  in  the  lungs  and  heart  that  must  be  sought  the  key  to 
correct  prognosis  in  chronic  disease,  and,  second,  that  heretofore  the 
prognosis  in  chronic  disease  has  been  of  too  gloomy  a  character.  The 
secret  of  successful  prognosis  is  to  form  an  opinion  of  the  bodily  con- 
dition as  accurate  as  it  is  possible  to  obtain,  and  then  to  estimate  the 
rate  at  which  the  disease  will  progress ;  for,  no  matter  how  incurable 
it  may  be,  it  must  become  worse  than  at  the  time  of  examination 
before  death  can  ensue. 


CHAPTER    XV. 

THE   TREATMENT   OF    CHRONIC    DISEASE. 

IN  the  preceding  chapter  it  has  been  shown  that  chronic  disease 
is  often  less  rapidly  fatal  than  is  commonly  taught,  that  complete  re- 
covery may  take  place,  and  even  that  incurable  disease  may  cease 
to  progress,  and  comfortable  health  continue  for  an  indefinite  period. 
Such  being  the  case,  it  is  time  to  take  a  more  hopeful  view  of  the 
treatment  of  chronic  disease  than  at  present  prevails.  With  abun- 
dant time  in  which  to  work,  it  is  under  such  circumstances,  if  ever, 
that  much  can  be  accomplished  by  treatment.  It  has  been  said  that 
the  treatment  of  typhoid  fever  is  unsatisfactory  if  there  is  no  one 
means  which  is  directly  applicable  to  its  cure  and  reliance  must  be 
placed  upon  general  management.  Nothing  could  be  more  unrea- 
sonable than  such  a  position,  if  it  can  be  shown  that  death  would 
sometimes  have  taken  place  but  for  the  intervention  of  the  physician. 
It  cannot  be  questioned  that  many  recover  from  typhoid  fever  with 
good  medical  advice  if  they  are  simply  kept  in  bed  and  on  appro- 
priate diet,  who  would  have  died  if  left  to  their  own  devices,  to  eat 
improper  food  or  starve  for  lack  of  appetite,  and  to  drag  themselves 
about  when  unfit  to  be  anywhere  but  in  bed.  It  is  by  such  simple 
means  as  these  in  the  first  place  that  wonderful  results  may  be  at- 
tained in  the  treatment  of  chronic  disease,  and  the  simpler  the  means 
the  greater  the  triumph  of  medicine.  Although  medicine  would  still 
have  a  field  and  the  treatment  of  disease  continue  to  be  useful  if  there 
were  no  drugs,  on  the  other  hand,  it  would  be  both  unreasonable  and 
untrue  to  say  that  their  use  does  not  lend  important  help  to  the  other 
means  applied  in  treatment.  While  acknowledging  the  value  of  drugs, 
it  is  necessary  to  exercise  great  care  not  to  overstate  the  truth,  for  the 
present  is  a  time  when  superstition  in  medicine  is  rife,  and  unreason 
masquerades  as  truth  with  a  boldness  that  was  not  surpassed  even 
in  the  days  when  bleeding  and  antimony  were  the  two  rival  specifics 
for  the  cure  of  all  disease,  and  when  their  respective  advocates  quar- 
relled with  a  bitterness  that  is  incomprehensible  unless  we  pause  to 
reflect  coolly  upon  some  of  the  follies  of  our  own  day.  A  medical 
journal — and  journals  reflect  the  opinions  of  the  time — issues  a 

205 


206  THE   ORIGIN   OF   DISEASE. 

solemn  editorial  upon  the  use  of  drugs,  and,  after  highly  recommend- 
ing a  dozen  newly  invented  chemicals,  which  have  not  been  in  exist- 
ence sufficiently  long  for  any  of  their  properties  to  be  known,  holds 
gentian  up  to  ridicule  as  an  inert  and  useless  substance  that  should 
be  banished  from  the  materia  medica.  This  is  unreasonable,  for  it  is 
well  known  that  dyspeptics  and  drunkards  crave  a  bitter  for  their  en- 
feebled stomachs,  experience  having  taught  them  its  benefits.  Among 
the  simple  bitters  none  has  a  higher  or  a  better  deserved  reputation 
than  gentian.  At  the  same  time  that  simple  but  useful  drugs  are 
decried,  many  others  are  advertised  as  having  specific  effects  for  the 
cure  of  one  disease  or  another,  although  it  should  be  well  known  that 
the  number  of  specifics  is  extremely  limited.  There  are  diseases  for 
which  a  specific  treatment  exists :  quinine  is  a  specific  for  the  treat- 
ment of  malarial  disease,  and  food  for  starvation ;  and  yet  all  cases 
cannot  be  saved.  Starvation  may  have  gone  so  far  that  food  will  not 
save  life.  The  condition  of  disease  produced  by  starvation  could  not 
be  more  simple  than  it  is,  and  there  cannot  be  the  slightest  difference 
of  opinion  in  regard  to  the  treatment  that  is  called  for,  and  its  general 
efficacy,  and  yet  the  patient  must  die.  This  seems  to  constitute  an 
answer  to  those  who  say  that  digitalis  is  a  useless  drug  because  it  fails 
to  cure  all  cases  of  heart  disease. 

For  the  treatment  of  chronic  disease  there  are  no  specifics,  and,  as 
there  is  such  an  infinite  variety  of  forms,  no  two  cases  being  exactly 
alike,  the  treatment  must  be  equally  varied.  It  is  often  very  difficult 
to  decide  what  treatment  should  be  applied  in  cases  like  those  de- 
scribed in  the  chapter  on  diagnosis,  which  are  without  definite  symp- 
toms, and  yet  suggest  strongly  that  there  soon  will  be  serious  disease, 
if  it  is  not  already  in  existence.  Under  the  circumstances  it  some- 
times seems  as  if  Bright's  disease  were  imminent,  or  there  are  vague 
"  gouty  tendencies,"  or  nothing  more  definite  can  be  ascertained  than 
that  the  patient  is  no  longer  in  a  state  of  bodily  perfection.  Such  a 
condition  is  so  common  that  it  must  often  occur  in  the  experience  of 
every  physician.  At  first  sight  it  seems  almost  hopeless  that  there 
can  be  any  successful  treatment,  when  everything  is  so  indefinite, 
but  reflection  brings  the  conclusion  that  the  situation  may  be  less 
bad  than  if  the  existence  of  organic  disease  were  certain,  and  clinical 
experience  shows  that  excellent  results  have  often  been  obtained 
when  they  were  least  expected.  As  no  objective  point  can  be  fastened 
upon  for  treatment  if  everything  is  indefinite,  it  has  seemed  to  me  that 
every  effort  should  be  directed  to  change  the  habit  of  body.  By  this 


THE   TREATMENT   OF   CHRONIC   DISEASE.  207 

is  meant  the  routine  into  which  the  functions  fall  with  the  advance  of 
life.  Just  as  there  are  personal  habits,  so  there  are  habits  of  body.  It 
is  in  the  middle-aged  or  older  persons  that  chronic  disease  is  most 
prevalent.  When  middle  age  is  reached,  most  persons  have  come  to 
live  in  a  routine  way ;  they  eat,  sleep,  and  work  in  the  same  way  day 
after  day,  and  the  organs  and  functions  go  on  in  a  circle  which  be- 
comes habitual  to  the  body.  When  health  fails  or  chronic  disease 
begins,  it  is  plain  that  the  imperfection  arose  owing  to  some  fault  in 
the  patient's  mode  of  living.  If  his  life  had  been  different  perhaps 
he  would  not  have  been  taken  sick.  What  should  be  done  to  cure 
the  imperfection  ?  Change  at  once  the  habit  of  body  which  allowed 
it  to  come,  and  as  radically  as  can  be  done  without  the  risk  of  injury. 
It  may  be  said  in  criticism  that  no  disease  has  been  named  and  no 
form  of  treatment  suggested,  and  therefore  that  all  this  is  so  vague  as 
to  be  worthless.  If  that  which  has  been  alleged  in  the  preceding 
chapters  is  true,  such  is  not  the  case,  and  those  who  have  com- 
prehended them  can  understand  what  is  meant  by  a  change  of  the 
habit  of  body.  Many  different  means  may  be  applied  to  change  the 
habit  of  body,  but  in  most  instances  less  will  be  attained  by  drugs 
than  by  management.  Most  important  methods  of  treatment  are 
change  of  locality  and  of  diet.  The  former  is  generally  within  the 
reach  only  of  the  well-to-do  or  rich,  and  should  not  be  recommended 
except  when  the  prospect  of  amendment  or  cure  is  sufficiently  great 
to  compensate  for  the  inconveniences  or  pecuniary  loss  attendant 
upon  a  change  of  dwelling.  The  benefit  to  be  derived  from  change 
of  diet  would  be  to  some  extent  within  the  reach  of  every  one,  were 
it  not  that  the  poorer  classes  are  generally  so  ignorant  that  they 
cannot  be  brought  to  understand  the  necessity  for  it,  and  without  the 
willing  assistance  of  the  patient  no  system  of  diet  can  long  be  carried 
out.  It  is  not  the  poor  alone  who  sin  in  this  regard,  for  often  it  is 
impossible  to  get  even  those  of  the  highest  intelligence  and  education 
to  submit  to  such  diet  and  rules  of  life  as  it  may  be  evident  would  be 
best  for  them.  It  is  very  difficult  to  curb  the  appetite  and  to  change 
the  habits,  and  to  attain  any  great  and  permanent  results  in  the  treat- 
ment of  disease  by  such  a  method  it  must  be  pursued  so  long  that 
the  stock  of  endurance  of  both  patient  and  physician  often  fails  before 
the  end  is  reached. 

It  is  very  difficult  to  treat  this  subject  systematically,  and  therefore 
my  discussion  of  it  may  be  somewhat  desultory.  The  range  of  dis- 
ease included  must  be  very  great,  as  it  has  been  pointed  out  again 


208  THE   ORIGIN   OF   DISEASE. 

and  again  that  chronic  disease  is  generally  wide-spread  in  its  effects, 
and  therefore  diseases  usually  considered  to  have  no  relations  to  one 
another  are  found  combined.  It  happens,  too,  that  a  case  may  be 
observed  through  its  entire  course,  and  when  it  has  ended  in  cure  it 
has  to  be  confessed  that  the  true  nature  of  the  disease  was  not  under- 
stood. If  it  is  possible,  however,  to  feel  assured  that  the  condition 
was  so  serious  as  to  threaten  life,  and  at  the  same  time  that  the  treat- 
ment pursued  was  instrumental  in  the  cure,  such  treatment  must  still 
be  looked  upon  as  satisfactory,  although  so  little  is  clear.  It  has 
been  said  that  an  important  part  of  the  treatment  of  chronic  disease 
is  to  change  the  habit  of  body.  When  a  man  begins  to  fail  and  it  is 
decided  that  it  is  more  than  the  mere  advance  of  years,  that  he  is 
sick,  and  yet  no  definite  disease  can  be  found  to  exist,  there  is  nothing 
that  can  be  reasonably  treated  by  drugs,  for  there  is  no  indication  to 
be  met.  Such  a  case  should  be  treated  by  being  sent  from  home 
for  a  greater  or  less  length  of  time,  or,  if  circumstances  forbid  this, 
advice  should  be  given  that  will  bring  about  a  change  in  the  mode 
of  life  at  home.  It  is  in  such  instances,  when  disease  has  not  yet 
reached  the  stage  of  organic  lesion,  that  baths  and  the  drinking 
of  waters  and  the  various  systems  pursued  at  cure  institutions  so 
often  prove  efficacious.  It  was  not,  however,  to  enter  into  a  lengthy 
discussion  of  such  matters,  which  have  been  better  described  by 
others,  that  this  chapter  was  written,  but  to  record  something  of 
my  personal  experience  in  the  treatment  of  chronic  disease,  and  my 
conclusions. 

Those  who  have  seen  much  of  chronic  disease  must  have  been 
impressed  by  the  surprising  prolongation  of  the  lives  of  some  of  the 
patients  and  the  complete  recovery  of  others.  In  the  hospitals  are 
seen  the  largest  number  of  bad  cases,  for  there  the  very  sick  congre- 
gate, while  in  private  practice  is  seen  another  aspect,  as  the  patients 
may  remain  for  years  under  observation  and  their  antecedents  be  well 
known.  Of  the  patients  who  recover  it  is  only  natural  to  ask  what 
influence  the  treatment  pursued  may  have  had  in  the  production  of 
the  result. 

It  is  a  common  experience  in  hospital  practice  that  patients  are 
brought  in  who  appear  to  be  in  the  last  stages  of  chronic  disease 
and  dying.  It  may  be  Bright's  disease  or  heart  disease  or  some 
other  of  the  various  complications  of  organic  disease  of  important 
organs.  A  common  combination  is  dropsy  with  heart  disease,  con- 
gestion of  the  lungs  or  slow  pneumonia,  albumen  and  casts  in  the 


THE   TREATMENT   OF   CHRONIC   DISEASE.  209 

urine,  and  orthopnoea  to  the  extent  that  the  unfortunate  sufferer  gasps 
for  every  breath  he  draws.  These  people  do  not  all  die,  although  at 
first  sight  and  to  all  except  those  who  have  had  experience  with  them 
it  seems  that  they  must.  In  some  cases  there  are  great  amelioration 
and  a  short  interval  of  freedom  from  suffering,  or  even  comfort,  before 
death  is  caused  by  a  relapse.  In  others  the  acute  symptoms  disappear 
and  the  patients  think  themselves  well,  especially  if  they  belong  to 
the  ignorant  classes,  who  are  hard  to  convince  that  their  health  is 
gone.  It  continues,  however,  to  be  plain  to  the  physician  that  there 
is  still  disease  of  important  organs  and  that  there  will  be  another 
attack.  These  people  go  from  a  hospital  and  take  up  their  work 
for  a  greater  or  less  length  of  time,  according  to  the  degree  of  their 
bodily  imperfection.  Sometimes  a  few  weeks  of  work  bring  on  an- 
other attack,  or  it  may  be  months  or  even  years,  but  the  attack  must 
come  if  the  physician  has  been  correct  in  his  diagnosis  and  has  based 
the  prognosis  on  solid  reason.  There  is  a  third  class  of  those  who 
recover,  in  whom,  after  the  acute  symptoms  have  passed  away,  no  in- 
dication of  organic  disease  can  be  found ;  they  sometimes  go  from  the 
hospital  seeming  to  be  well,  and  may  continue  so  indefinitely.  There 
can  be  no  reasonable  doubt  that  many  of  those  who  recover  in  the 
hospitals  would  have  died  if  they  had  remained  in  their  own  homes, 
for  at  home  they  continued  to  go  from  bad  to  worse,  and  within  a 
short  time  after  removal  to  a  hospital  improvement  often  begins.  It 
was  the  treatment  that  produced  the  result,  and  by  treatment  is  meant 
everything  that  was  done  for  the  patient.  If  the  term  treatment  is 
used  so  comprehensively  it  includes  many  things,  and  in  order  to 
make  treatment  as  good  as  possible  it  is  necessary  to  sift  out  among 
these  many  things  that  which  is  beneficial  from  that  which  is  useless. 
If  examined  from  one  point  of  view  the  ordinary  treatment  of  chronic 
disease  which  is  pursued  at  the  present  day  is  almost  infinitely  various, 
while  from  another  it  presents  wonderful  sameness.  It  is  in  regard  to 
the  use  of  drugs  that  differences  of  opinion  exist,  while  as  concerns 
general  management  there  is  a  fairly  satisfactory  agreement.  Con- 
cerning drugs  the  preceding  statement  must  be  qualified  so  far  as  to 
say  that  there  are  a  few  of  them  which  have  been  long  in  use  and 
whose  beneficial  effects  are  so  generally  conceded  that  their  useful- 
ness may  be  said  to  have  passed  beyond  the  range  of  dispute.  The 
present  is  a  time  of  many  medicines ;  new  chemicals  are  made  and 
vegetable  substances  are  introduced  with  a  rapidity  that  is  startling. 
One  year,  patients  with  dropsy  and  oppression  are  salivated  and 

14 


210  THE   ORIGIK  OF   DISEASE. 

sweated  with  jaborandi ;  another,  fever,  no  matter  what  may  be  its 
cause,  is  reduced  by  large  doses  of  antipyretics ;  a  third,  nitroglycerin 
is  said  to  have  marvellous  properties  in  the  treatment  of  diseases 
involving  disturbance  of  the  circulation,  and,  as  the  circulation  is 
affected  in  almost  every  form  of  sickness,  the  range  of  the  reputed 
field  of  usefulness  of  the  drug  is  almost  without  limit.  It  is  only  a 
few  years  since  the  world  of  medicine  was  disturbed  by  a  clamor  that 
the  injection  of  sulphuretted  hydrogen  gas  into  the  rectum  was  bene- 
ficial in  the  treatment  of  consumption,  and  for  a  few  months  this  ab- 
surdity was  credited  to  such  an  extent  that  medical  journals  were  filled 
with  accounts  of  the  relief  and  cure  of  consumptives  by  it.  To  any 
reasonable  mind  not  preoccupied  by  the  search  for  new  medicines  the 
fallacy  of  this  restless  desire  for  novelty  is  evident.  More  would  be 
accomplished  if  the  same  time  were  devoted  to  trying  to  attain  greater 
perfection  in  the  management  of  drugs  already  known  to  be  of  use, 
for  there  is  still  room  for  very  great  improvement  in  this  direction. 
It  is  impossible  that  drugs  that  are  so  lauded  for  a  year  or  two  and 
then  forgotten  can  be  of  great  value,  and  when  one  remembers  the 
prostration  that  follows  the  salivation  and  sweating  produced  by  jabo- 
randi, or  the  equally  powerful  effects  of  other  medicines  that  are 
used,  there  is  no  escape  from  the  thought  that,  if  no  benefit  is  obtained, 
it  is  certain  that  harm  is  done.  In  regard  to  the  use  of  drugs  one 
principle  has  so  deeply  impressed  itself  upon  me  that  my  opinion  is 
very  fixed.  It  is  that  when  the  use  of  moderate  and  ordinary  doses 
is  ineffectual,  large  doses  will  generally  prove  equally  so,  if  not  inju- 
rious. Sometimes  large  doses  given  for  a  short  time,  to  tide  over  an 
emergency,  may  be  useful,  but  when  they  must  be  long  continued 
they  generally  are  inefficacious.  The  failure  is  for  the  same  reason 
probably  as  that  for  which  food  will  not  always  cure  starvation, 
although  it  is  the  specific.  The  disease  induced  has  gone  so  far  as  to 
be  incurable.  If  an  ordinary  dose  of  a  drug  produces  no  good  effect 
and  a  large  one  does  no  better,  it  by  no  means  shows  that  the  medi- 
cine is  always  useless,  for  the  case  may  be  one  too  far  gone  for  help. 
The  belief  has  been  expressed  that  treatment  of  chronic  disease  often 
directly  brings  about  a  cure,  and  at  the  same  time  it  has  been  shown 
that  much  of  the  drugging  that  is  now  in  vogue  is  useless,  if  not 
injurious.  If  such  be  the  case,  it  is  some  other  portion  of  the  treat- 
ment that  brings  about  the  result.  Dropsy  with  oppression  has  been 
mentioned  as  a  type  of  chronic  disease,  and  patients  so  affected  are 
usually  kept  in  bed  and  on  milk  diet ;  the  circulation  is  supported  by 


THE   TREATMENT   OF   CHRONIC   DISEASE.  211 

digitalis  and  stimulants,  opium  is  given  to  soothe,  the  state  of  the 
functions  and  excretions  is  examined,  and  such  medicines  as  may  help 
their  efficiency  of  action  are  given.  This  is  the  treatment  that  cures 
chronic  disease,  or,  if  it  has  passed  beyond  the  possibility  of  cure, 
gives  a  temporary  reprieve,  or,  in  the  worst  cases,  at  least  alleviates 
the  suffering. 

It  is  not  desirable  in  a  work  like  this  to  discuss  at  length  the 
treatment  of  chronic  disease,  for  it  would  necessitate  the  writing  of 
a  complete  treatise  on  therapeutics.  My  desire  is  to  express  my 
disapproval  of  the  excessive  use  of  new  drugs  whose  effects  cannot 
be  understood  because  they  have  not  been  known  sufficiently  long, 
and,  on  the  other  hand,  to  express  my  conviction  of  the  value  of  that 
treatment  of  chronic  disease  which  is  based  upon  common  sense 
and  experience.  Years  of  trial  have  brought  to  me  the  conviction 
that  many  cases  that  would  have  died  without  it  are  relieved  or  re- 
cover under  a  treatment  consisting  of  a  suitable  regimen,  appropriate 
diet,  attention  to  the  functions  and  secretions,  and  the  use  of  medi- 
cines like  digitalis,  opium,  stimulants,  and  many  others.  The  treat- 
ment which  is  most  successful  is  that  which  has  been  called  sympto- 
matic, and  this  is  not  difficult  to  understand  when  it  is  recollected  that 
chronic  disease  is  wide-spread  in  its  effects  and  the  lesions  are  often 
incurable,  in  which  case  the  utmost  that  can  be  accomplished  is  to 
get  the  organism  into  such  a  condition  that  life  may  continue,  and,  if 
possible,  in  comfort.  The  treatment  which  will  accomplish  most  in 
chronic  disease  has  now  been  outlined,  and  the  opinion  that  a  more 
hopeful  view  of  treatment  should  be  taken,  as  it  effects  much  more 
than  the  pessimistic  concede,  has  been  elaborated. 

Another  class  of  chronic  disease  may  be  formed,  of  cases  having 
demonstrable  disease  of  grave  form,  but  as  yet  at  an  early  stage.  In 
such  cases  it  is  important  to  ascertain  whether  there  is  organic  lesion 
besides  that  of  which  it  is  possible  to  be  certain,  and  most  important 
of  all  is  the  question  what  treatment  should  be  instituted  to  cure,  or, 
if  cure  be  unattainable,  to  prolong  life  and  comfort  to  the  utmost 
possible.  The  condition  it  is  intended  to  designate  cannot  better  be 
made  plain  than  by  the  description  of  a  case  representative  of  one 
form  of  it.  A  man  about  sixty  years  of  age,  who  weighed  a  little 
more  than  two  hundred  pounds  and  whose  boast  was  that  he  had 
never  known  a  day's  sickness,  was  taken  with  extreme  irregularity  of 
the  heart.  He  had  quite  frequent  attacks  of  vertigo,  during  which  he 
never  fell,  although  his  lips  were  blue,  and  he  became  subject  to  diar- 


212  THE   ORIGIN   OF   DISEASE. 

rhcea,  which  was  very  prostrating  but  did  not  deprive  him  of  appetite. 
He  had  lived  an  active  life,  and,  having  an  excellent  appetite,  ate  freely, 
probably  largely,  and  of  rich  food,  but  drank  almost  nothing, — 
never  taking  spirits,  and  seldom  wine,  and  then  only  in  the  greatest 
moderation.  The  irregularity  of  the  heart  was  violent  and  persistent, 
but  no  other  direct  evidence  of  disease  was  discovered,  although  it 
may  almost  certainly  be  inferred  that  fibroid  changes  of  many  of  the 
organs,  especially  of  the  kidneys,  exist.  At  the  present  time,  after  ten 
or  twelve  years,  the  patient,  being  over  seventy,  is  living  and  still  in 
active  business.  During  the  whole  of  the  period  which  has  elapsed 
since  he  was  taken  sick  the  heart  has  always  been  violently  irregular, 
although  it  has  been  less  tumultuous  in  its  action  during  the  last  year 
or  two  than  previously.  He  has  been  subject  to  diarrhoea,  and  twice 
has  had  slight  catarrhal  pneumonia.  His  weight  has  fallen  from  two 
hundred  and  twenty  to  one  hundred  and  eighty  pounds,  and  he  con- 
tinues in  perfect  comfort  and  enjoyment  of  life.  An  outline  of  the 
case  having  been  given,  the  treatment  will  now  be  described,  and  it 
does  not  seem  possible  to  think  otherwise  than  that  it  has  had  a  great 
influence  in  effecting  the  prolongation  of  life.  At  the  beginning  of 
the  illness  this  man  was  directed  to  avoid  physical  effort  as  much  as 
possible,  to  ride  whenever  he  could,  and  to  walk  only  when  he  was 
obliged  to,  and  then  as  short  distances  as  possible  and  slowly.  He 
was  advised  to  go  to  his  place  of  business  only  once  a  day,  going 
both  to  and  from  his  home  in  a  carriage  or  in  the  public  conveyance, 
and,  after  taking  his  mid-day  meal  at  home,  to  rest  or  sleep  and  read 
in  the  afternoons,  except  in  the  summer  months  when  driving  in  a 
carriage  is  agreeable.  The  diet  was  very  important,  and  required  care- 
ful regulation.  It  was  explained  to  him  that,  as  he  was  unfit  to  take 
exercise,  a  less  amount  of  food  would  be  required  than  when  he  had 
been  more  active.  At  the  same  time  he  was  told  that  all  sorts  of 
fancy  articles  of  food,  which  he  was  very  fond  of  and  had  indulged  in 
freely,  would  be  injurious  ;  that  they  were  nearly  as  bad  as  the  overuse 
of  spirits.  Pies,  puddings,  and  cakes  were  all  interdicted,  and  he  was 
told  to  eat  only  the  simpler  articles  of  food,  and  that  he  might  safely 
take  any  of  these.  With  such  a  patient  it  is  unwise  to  make  the 
regulations  too  stringent,  for  if  the  appetite  is  not  allowed  some  nat- 
ural gratification  life  becomes  so  irksome  that  medical  directions  are 
thrown  to  the  winds.  This  man  was  told  to  eat  a  light  evening  meal, 
consisting  simply  of  bread  and  butter  and  tea,  or  occasionally,  if  this 
was  so  tiresome  as  to  be  unbearable,  to  add  to  it  one  simple  dish,  but 


THE   TREATMENT   OF   CHRONIC   DISEASE.  213 

to  restrain  the  appetite.  At  mid-day  was  taken  the  best  meal,  and  at 
that  time  he  was  told  to  eat  as  much  as  he  wanted,  but  that  it  should 
be  simple  and  not  varied  beyond  certain  limits.  The  mid-day  dinner 
has  consisted  of  soup  and  a  simple  joint  with  only  two  vegetables, 
and,  as  an  ordinary  thing,  no  dessert.  A  dessert  like  rice-pudding 
might  be  taken  occasionally  when  the  desire  for  it  could  no  longer 
be  resisted.  Breakfast  was  to  consist  of  bread,  coffee,  eggs,  and  a 
simple  dish  of  meat.  The  patient  was  instructed  that  what  he  needed 
was  a  reduction  of  the  quantity  of  food  taken,  that  he  was  to  cease 
the  use  of  desserts  and  rich  dishes,  and  that  it  was  exceedingly  im- 
portant to  make  the  evening  meal  a  very  light  one.  He  was  told  that 
it  was  not  important  for  him  to  cease  eating  beef  because  mutton  was 
less  gouty,  or  to  confine  himself  to  poultry  because  red  meats  had 
some  specifically  bad  effects. 

A  great  deal  of  stress  is  often  laid  by  physicians  upon  the  evil 
effects  of  beef,  which  is  said  to  be  gouty.  It  is  probable  that  the 
ill  effect  of  meat  is  much  exaggerated,  and  medical  directions  often 
fail  because  persons  are  advised  to  avoid  eating  meat  when  their  real 
need  is  a  general  reduction  of  their  daily  food.  If  a  patient  is  told  to 
dine  at  mid-day  upon  soup,  joint,  and  two  vegetables,  the  dinner  is 
good  enough,  and  yet,  being  simple,  the  risk  of  over-eating  is  not  very 
great.  On  the  other  hand,  if  ordered  to  eat  no  red  meat,  but  to  take 
in  its  stead  only  poultry  and  fish,  persons  soon  become  so  disgusted 
that  it  is  impossible  to  eat  at  all,  and  all  advice  is  thrown  aside.  The 
directions,  therefore,  for  the  diet  were  that  the  breakfast  and  dinner 
should  be  simple,  and  the  dinner  eaten  at  mid-day  instead  of  at  night, 
and  that  the  evening  meal  should  be  of  the  simplest  possible  nature, 
and  very  little  eaten  at  that  time.  No  restriction  was  placed  upon  the 
quantity  to  be  eaten  at  breakfast  and  dinner,  but  only  upon  the  number 
of  dishes,  and  all  rich  and  fancy  food  was  prohibited.  There  is  good 
reason,  founded  upon  experience,  for  believing  that  the  mixture  of 
many  different  kinds  of  food  at  one  meal  has  a  bad  effect  upon  the 
system,  especially  if  the  practice  be  long  continued.  This  patient  was 
given  a  prescription  for  ten  drops  of  tincture  of  digitalis  and  two  and 
a  half  grains  of  carbonate  of  ammonium.  The  medicine  was  taken  for 
a  good  while  after  the  commencement  of  the  illness  four  times  a  day, 
and  since  that  time,  during  the  whole  period  of  more  than  ten  years, 
the  patient  seldom  passes  a  day  without  it.  Generally  he  takes  two 
doses  a  day,  one  after  breakfast  and  the  second  at  bedtime,  but  if  the 
heart  is  more  irregular  than  usual,  or  he  has  giddiness  or  is  weak,  he 


214  THE   ORIGIN   OF   DISEASE. 

takes  three  or.  four  doses,  according  to  the  circumstances.  A  number 
of  times  the  digitalis  and  carbonate  of  ammonium  were  withdrawn,  but 
on  each  occasion  the  patient  was  less  well  and  their  use  was  promptly 
resumed.  At  the  present  time  this  man  enjoys  very  satisfactory 
health,  the  heart  being  less  irregular  than  it  was  some  years  ago, 
although  even  now  there  never  are  many  regular  successive  beats. 
No  reasonable  physician  of  experience  can  doubt  that  this  patient  has 
organic  disease  of  the  heart,  and  the  inference  is  a  fair  one  that  the 
nature  of  this  is  degeneration  of  the  muscular  substance,  probably  of 
some  one  of  the  forms  described  in  the  chapter  on  the  heart,  and  that 
there  is  disease  of  the  blood-vessels.  Disease  of  the  blood-vessels  is 
often  a  most  important  element  in  heart  disease,  and  it  has  been  shown 
(Figs.  4  and  5)  how  it  may  be  of  such  a  form  as  to  cut  off  the  sup- 
ply of  blood  and  thus  starve  the  organ.  If  there  is  any  truth,  how- 
ever, in  what  has  been  so  often  already  said  of  the  manner  in  which 
chronic  disease  spreads  over  a  wide  extent,  and  especially  in  the  old, 
who  are  as  naturally  fibroid  as  old  trees  are  naturally  brittle,  it  is 
a  matter  almost  of  certainty  that  the  man  whose  history  has  been 
described  has  other  organic  disease  besides  that  of  the  heart  which 
revealed  itself  by  the  objective  sign  of  excessive  and  long-continued 
irregularity.  Precisely  what  this  may  be  is  a  question  of  diagnosis, 
and  therefore  not  suitable  for  discussion  in  this  chapter,  it  being  suffi- 
cient for  the  present  purpose  to  keep  in  mind  that  the  disease  is  not 
confined  to  the  heart.  It  will  be  well,  before  leaving  the  case,  to  dwell 
upon  the  important  points  of  the  treatment.  The  treatment  ranges 
itself  naturally  under  three  heads, — regimen,  diet,  and  medicine, — 
and  it  is  difficult  to  say  that  one  is  more  important  than  another,  for 
they  are  essentially  supporting  to  one  another,  and  no  one  of  them 
is  capable  of  effecting  its  best  results  without  the  help  of  the  others. 
Much  has  been  written  of  late  years  in  regard  to  the  need  of  exercise 
for  the  cure  of  organic  heart  disease,  and  in  some  cases  mountain- 
climbing  has  been  recommended  for  this  purpose.  No  one  will  ques- 
tion that  rest  in  bed  is  an  essential  part  of  good  treatment  of  some 
forms  and  stages  of  heart  disease,  and  that  in  others  as  quiet  a  daily 
routine  as  possible  and  the  avoidance  of  physical  effort  are  essential. 
Even  if  it  be  conceded,  therefore,  that  an  active  life  with  regular  exer- 
cise is  sometimes  best,  it  is  certain  that  at  other  times  the  greatest 
possible  degree  of  quietude  is  essential.  The  conviction  has  long 
since  come  to  me  that  in  a  case  such  as  the  one  described,  an  old  man 
with  irregular  heart  and  giddiness  and  becoming  less  strong,  the  only 


THE   TREATMENT   OF   CHRONIC   DISEASE.  215 

wise  course  is  to  obtain  for  such  a  patient  the  greatest  possible  amount 
of  quiet.  A  day  or  two  in  bed  occasionally  would  have  been  very 
beneficial,  but  the  patient  is  a  very  stirring  man,  and  would  fret  to 
such  a  degree  if  kept  in  bed  that  such  a  course  would  have  been  im- 
possible. The  reason  so  much  emphasis  is  laid  upon  the  necessity 
for  the  advice  that  was  given,  to  avoid  effort  so  much  as  never  to 
walk  when  it  was  possible  to  ride,  is  that  it  seems  to  me  that  it  was 
probably  more  important  than  any  other  one  thing  in  the  successful 
management  of  the  case.  Had  this  patient  not  been  warned  against 
the  dangerous  effects  of  the  active  life  which  he  loved,  and  which  he 
gave  up  only  because  warned  in  such  a  way  that  he  was  convinced  of 
the  need  for  quiet,  there  can  be  little  reasonable  doubt  that  his  strug- 
gling heart  would  have  failed  and  he  would  have  been  long  since 
dead.  Quietude,  therefore,  was  an  essential  of  the  treatment.  The 
treatment  of  heart  disease  by  exercise  when  it  is  clear  that  there  is 
organic  lesion  of  progressively  degenerative  nature  seems  to  me  a 
dangerous  method  and  capable  of  doing  great  harm  in  many  cases. 
On  the  other  hand,  well-regulated  exercise  for  the  cure  of  nervous  dis- 
turbance of  the  heart  is  so  certainly  useful  as  to  require  no  argument 
in  its  favor.  It  has  already  been  said  that  cardiac  murmurs  indicating 
that  injury  of  the  valves  has  occurred  are  often  unimportant,  and  cer- 
tainly less  important  than  disease  of  the  heart-walls.  Such  murmurs 
result  from  attacks  of  acute  inflammation,  rheumatism  being  the  type 
of  disease  which  most  often  causes  them.  After  an  attack  of  acute 
endocardial  inflammation  the  distortion  of  a  valve-leaflet  which  pro- 
duces a  murmur  may  be  almost  disregarded  in  treatment  if  the  walls 
of  the  heart  continue  sound,  and  exercise  to  any  reasonable  extent 
may  be  recommended.  Cases  of  this  nature  are  of  frequent  occur- 
rence, especially  among  young  persons,  and  formerly,  when  less  well 
understood  than  at  present,  they  were  thought  more  serious  than 
they  are,  so  that  those  suffering  with  them  were  subjected  to  treat- 
ment that  was  unnecessary,  and  many  useless  precautions  were  taken. 
When  the  general  condition  is  good  no  treatment  is  required  under 
the  circumstances.  It  is  highly  probable  that  it  is  cases  of  this  nature 
that  have  improved  under  the  mountain-climbing  treatment.  The 
importance  of  appropriate  diet  in  a  case  like  the  one  under  considera- 
tion can  hardly  be  over-estimated.  Any  one  who  has  had  the  charge 
of  animals  knows  how  their  condition  can  be  changed  by  the  quantity 
and  nature  of  the  food.  If  the  appetite  is  good,  it  is  generally  an  easy 
matter  to  make  a  horse  or  a  dog  fat  or  lean  at  will  by  the  manage- 


216  THE   ORIGIN   OF   DISEASE. 

ment  of  the  food.  The  patient  was  a  man  with  a  large  appetite,  and 
his  habit  had  been  to  eat  much  and  of  rich  and  fattening  food.  It 
became  necessary  on  account  of  his  heart  to  stop  his  activity,  and 
therefore  his  diet  had  to  be  made  to  fit  the  changed  circumstances, 
besides  which  it  was  almost  certain  that  the  quantities  and  cloying 
nature  of  the  things  he  had  habitually  eaten  were  in  excess  of  what 
his  system  could  dispose  of  and  maintain  itself  in  good  condition ; 
therefore  the  food  had  had  an  influence  in  producing  disease.  It  was 
very  evident  that  there  were  two  important  things  to  be  done, — to 
reduce  the  quantity  of  food  and  to  stop  the  eating  of  rich  and  un- 
wholesome things.  Being  a  hungry  man,  it  could  not  be  expected 
that  he  would  at  once  change  his  habits  and  reduce  his  food  beyond  a 
certain  reasonable  point,  therefore  it  was  expedient  to  allow  him  to 
eat  as  much  as  he  wished  at  breakfast  and  mid-day,  and  to  effect 
the  needed  reduction  in  quantity  of  food  by  limiting  the  number  of 
things  to  be  eaten  at  one  meal  and  allowing  only  wholesome  and 
plainly  cooked  food.  Not  many  men  have  so  strong  an  appetite  as  to 
over-eat  when  the  food  is  plain  and  the  dishes  are  few.  Experience 
has  convinced  me  that  persons  with  disease  such  as  the  patient  had 
are  greatly  benefited  by  making  the  evening  meal  a  very  light  one. 
No  reason  can  be  given  for  this,  but  it  is  a  fact  established  by  obser- 
vation and  is  very  important.  The  light  evening  meal  will  be  found 
to  be  a  great  help  toward  cure,  and  most  reasonable  patients  can  be 
induced  to  submit  to  it,  if  only  the  advice  given  in  regard  to  what 
should  not  be  eaten  at  other  times  is  not  made  too  stringent.  In 
recommending  any  system  of  diet  it  is  necessary  to  study  the  char- 
acter of  the  patient  and  try  to  estimate  the  degree  of  his  self-con- 
trol, making  the  rules  elastic  to  suit  the  case,  so  as  not  to  ask  for 
an  amount  of  self-denial  of  which  the  person  is  incapable.  A  diet 
may  be  theoretically  good  but  practically  unattainable.  The  eating  of 
meat  alone  has  been  recommended  for  the  treatment  of  diabetes.  If 
there  are  people  in  the  temperate  regions  of  the  world  who  could  live 
for  any  length  of  time  upon  meat  alone,  they  are  very  few,  and  it  is 
not  worth  while  to  recommend  it  as  a  system,  for  it  is  impracticable. 

Except  for  short  intermissions,  the  patient  whose  case  has  been  de- 
scribed has  taken  digitalis  and  carbonate  of  ammonium  during  more 
than  ten  years.  Experience  in  the  treatment  of  cases  of  heart  disease 
has  convinced  me  that  digitalis  and  carbonate  of  ammonium,  given  in 
the  doses  that  have  been  mentioned,  are  important  adjuncts  to  diet 
and  regimen.  Large  doses  are  not  often  prescribed,  except  in  cases 


THE   TREATMENT   OF   CHRONIC   DISEASE.  217 

which  seem  immediately  to  threaten  life,  and  under  such  circumstances 
not  so  much  is  to  be  expected  as  in  less  severe  conditions,  when  there 
is  more  time  in  which  to  work.  Large  doses  generally  seem  less 
beneficial  and  produce  less  satisfactory  results  than  moderate  ones : 
this  is  pre-eminently  true  of  digitalis.  Great  quantities  of  it  may 
sometimes  seem  to  help  in  tiding  over  an  emergency,  but  when  the 
condition  appears  so  desperate  that  the  physician  feels  impelled  to 
continue  the  administration  of  large  doses  of  digitalis  for  a  long  time, 
it  soon  comes  about  that,  in  studying  the  state  of  the  patient,  it  is  im- 
possible to  be  sure  whether  some  of  the  bad  symptoms  are  caused  by 
the  disease  or  are  due  to  the  great  quantities  of  the  medicine.  To 
illustrate  what  is  meant:  a  patient  under  my  charge  with  organic  heart 
disease  had  been  given  fifteen  minims  of  tincture  of  digitalis  every  two 
hours  for  more  than  a  week.  The  amount  taken  daily,  therefore,  was 
three  drachms  of  the  tincture,  making  more  than  two  and  a  half  ounces 
in  a  week.  Estimating  that  each  fluidrachm  of  the  tincture  is  equiva- 
lent to  eight  grains  of  powdered  digitalis,  twenty-four  grains  were 
taken  daily,  and  two  and  four-fifths  drachms  of  the  powdered  drug 
within  one  week.  It  is  rather  surprising,  and  contrary  to  much  of  the 
usual  teaching,  that  a  man  could  take  so  great  an  amount  of  digitalis 
and  live,  and  the  fact  is  worth  remembering,  for  it  makes  it  probable 
that  more  digitalis  is  required  to  kill  than  is  generally  supposed.  The 
therapeutic  puzzle  presented  by  this  patient  at  the  end  of  the  week 
when  he  came  into  my  charge  was  very  difficult  to  disentangle.  The 
cardiac  action  was  weak,  intermitting,  and  irregular  in  the  highest 
degree,  there  was  constant  vomiting,  and  the  patient  was  bathed  in 
cold  sweat  so  that  he  appeared  to  be  almost  in  collapse.  Scientific 
therapeutists,  who  have  studied  the  mode  of  death  from  poisonous 
doses  of  digitalis,  say  that  as  the  poisoning  goes  on  the  heart  con- 
tracts more  and  more  firmly,  then  the  muscular  spasm  becomes  so 
great  that  the  ventricles  no  longer  dilate  fully  during  diastole.  The 
ventricles  dilate  less  and  less,  and  finally  death  takes  place  with  the 
heart  tightly  contracted  and  almost  empty  of  blood.  Pathologists 
know  that  in  cases  like  that  described,  in  which  the  heart  is  generally 
large  and  heavy  and  the  walls  organically  degenerated,  it  is  common 
to  find  after  death  that  the  heart  is  fully  open,  all  the  cavities  being 
distended  to  their  greatest  capacity  with  blood  which  is  more  or  less 
clotted.  It  is  easy  to  draw  the  conclusion  that  for  some  time  before 
death  under  these  circumstances  exactly  the  opposite  of  what  happens 
in  digitalis  poisoning  obtains :  the  heart  is  filled  with  blood,  some  of 


2i8  THE   ORIGIN   OF   DISEASE. 

which  is  already  clotted,  and  the  muscular  action  is  feeble,  so  that  at 
each  contraction  only  a  little  blood  is  expelled  and  none  of  the  cavities 
are  ever  emptied.  Which  of  these  states  of  the  heart  and  circulation 
existed  in  the  man  who  had  taken  large  doses  of  digitalis  for  a  week, 
and  what  treatment  did  he  require?  As  there  has  never  been  much 
opportunity  to  watch  how  death  would  take  place  if  a  man  with  an 
enlarged  and  degenerated  heart  were  poisoned  with  digitalis,  most  of 
Avhat  is  known  of  the  mechanism  of  digitalis  poisoning  having  been 
learned  from  the  observation  of  it  in  animals  with  healthy  hearts,  it  is 
impossible  to  know  what  effect  the  drug  does  produce  upon  a  heart 
diseased  like  that  of  the  man  whose  condition  has  been  described. 
For  the  clinician  there  was  only  one  reasonable  conclusion  :  the  patient 
had  had  digitalis  enough.  The  large  quantity  taken  had  failed  to  do 
any  good,  and  if  the  use  of  any  digitalis  had  been  continued  it  would 
have  been  impossible  to  be  certain  that  the  bad  symptoms  were  not 
partly  due  to  digitalis  poisoning.  It  was  directed  that  the  patient 
should  lie  as  still  as  possible,  and  should  take  every  two  hours  an 
ounce  and  a  half  of  milk,  with  half  an  ounce  of  lime  water  and  two 
fluidrachms  of  brandy.  A  quarter  of  an  hour  later  was  given  one- 
sixteenth  of  a  grain  of  sulphate  of  morphine,  with  two  minims  of 
chloroform,  and  a  teaspoonful  of  compound  tincture  of  cardamom,  in 
a  little  water.  All  other  medicine  and  food  were  forbidden,  and  in- 
structions were  given  that  the  greatest  regularity  was  to  be  observed 
in  the  administration  of  the  liquid  nourishment  and  medicine,  that 
they  were  to  be  given  regardless  of  whether  the  patient  vomited  imme- 
diately before  or  after  them,  and  that  nothing  else  was  to  be  tried  for 
some  time,  even  if  the  vomiting  continued  to  such  a  degree  that  it 
seemed  as  if  everything  taken  into  the  stomach  was  ejected.  In  the 
course  of  a  day  or  two  the  vomiting  and  cold  sweating  ceased,  but 
the  heart  continued  to  be  irregular,  although  it  improved  in  strength. 
It  was  many  weeks  before  the  patient  gathered  strength  enough  to 
be  able  to  sit  up,  but  finally  he  was  discharged  from  the  hospital 
in  a  comfortable  condition,  although  still  suffering  with  heart  dis- 
ease to  such  a  degree  that  it  seemed  unlikely  he  could  live  very 
long.  The  history  has  been  narrated  to  show  how  ineffectual  even 
the  largest  doses  of  digitalis  proved  in  a  case  in  which  recovery  from 
the  acute  attack  took  place  under  the  use  of  soothing  and  mildly 
stimulating  medicines,  careful  regulation  of  the  food,  and  profound 
rest.  It  is  instructive  also  to  notice  how  the  difficulty  of  attaining  a 
correct  judgment  of  the  case  was  made  greater  because  of  the  prob- 


THE   TREATMENT   OF   CHRONIC   DISEASE.  219 

ability  that  the  symptoms  were  partly  due  to  poisoning  by  the  medi- 
cine, and  the  impossibility  of  distinguishing  what  might  be  the  symp- 
toms of  poisoning  from  the  symptoms  of  the  disease.  It  illustrates 
how  large  doses  of  medicine  may  fail  to  benefit  or  may  even  do  harm, 
just  as  the  case  of  long-standing  irregularity  of  the  heart  in  an  old 
man  illustrates  the  usefulness  of  small  doses  of  digitalis  continued  for 
a  long  period.  This  leads  to  an  important  question :  How  much 
digitalis  can  with  advantage  and  safety  be  continued  for  a  long  time  ? 
The  result  of  my  reading  and  experience  has  been  the  formation  of 
the  opinion  that  ten  drops  of  tincture  of  digitalis  may  be  given  three 
times  a  day  as  long  as  may  seem  desirable,  even  for  a  year  or  more, 
but  not  more  than  this  dose  unless  the  patient  is  kept  constantly 
under  medical  supervision,  so  that  it  may  be  stopped  if  desirable. 
This  statement  may  seem  somewhat  dogmatic,  but  it  is  necessary 
to  set  dogmatic  standards  in  dosage,  and  the  amount  named  will  be 
found  a  fitting  one  in  cases  in  which  there  is  no  idiosyncrasy.  In 
connection  with  what  has  been  related  of  the  patient  to  whom  large 
doses  of  digitalis  had  been  ineffectually  given  it  may  be  well  to  dwell 
upon  the  good  results  that  were  obtained  from  opium,  and  to  say  how 
very  useful  it  often  is  in  cases  of  chronic  disease  in  which  there  is 
pain  or  great  nervous  disturbance  of  almost  any  kind.  This  is  espe- 
cially true  of  heart  disease.  If  there  is  vomiting  in  addition  to  the 
other  sufferings  common  in  heart  disease,  the  use  every  two  hours 
of  one-sixteenth  of  a  grain  of  sulphate  of  morphine,  and  two  minims 
of  chloroform,  in  a  teaspoonful  of  compound  tincture  of  cardamom  or 
other  aromatic  containing  alcohol  enough  to  dissolve  the  chloroform, 
is  often  most  efficacious.  Doses  as  large  as  these  must  of  course 
be  given  only  so  long  as  the  patient  is  under  constant  supervision, 
and  generally  should  not  be  continued  beyond  a  week  or  two.  The 
doses  of  opium  and  how  it  should  be  used  in  disease  are  not 
fixed  in  text-books  in  such  a  way  as  to  make  it  easy  for  one  seeking 
information  to  understand.  For  instance,  the  United  States  Dis- 
pensatory (edition  of  1883,  page  1076),  in  advising  in  regard  to  the 
dose  of  opium,  mentions  that  as  little  as  one-fourth  or  one-third  of  a 
grain  is  sometimes  given,  and  then  adds, "  in  acute  peritonitis  we  have 
seen  the  equivalent  of  seventy-five  grains  given  during  the  twenty- 
four  hours  with  advantage."  Finally,  it  says,  "  The  ordinary  dose  of 
dried  or  powdered  opium  may  be  set  down  as  one  grain."  The  ad- 
visability of  ever  giving  as  much  as  seventy-five  grains  of  opium  in 
twenty-four  hours  is  a  matter  in  regard  to  which  physicians  would 


220  THE   ORIGIN  OF   DISEASE. 

greatly  differ,  while  the  other  doses  mentioned  are  beyond  question 
such  as  are  usually  fitting  and  beneficial.  The  advice,  however,  is 
insufficient,  for  it  is  not  stated  how  much  should  be  given  in  cases  of 
chronic  disease  or  in  other  conditions  in  which  it  is  deemed  that  bene- 
fit would  accrue  from  its  soothing  or  supporting  or  other  effect.  It 
is  very  desirable  that  clinicians  should  have  some  fixed  standard  of 
dosage  of  opium  parallel  with  that  which  has  been  fixed  for  digitalis. 
It  ought  to  be  generally  known  how  much  may  be  given  continuously 
for  several  weeks  without  passing  what  is  called  by  therapeutists  the 
physiological  limit  and  producing  poisonous  effects.  Having  care- 
fully studied  this  matter  and  having  often  watched  the  effects  of  the 
quantities  to  be  named,  I  feel  warranted  in  stating  that  the  ordinary 
human  adult  can  take  one-quarter  of  a  grain  of  powdered  opium,  or 
ten  drops  of  laudanum,  every  two  hours  for  several  weeks  succes- 
sively, and  there  will  be  no  contraction  of  the  pupils,  no  unusual 
sleepiness,  nor  any  other  symptom  of  the  narcotic  effects  of  the  drug. 
These  doses  equal  three  grains  in  each  twenty-four  hours,  or,  if  laud- 
anum be  used,  four  grains,  if  the  estimate  is  correct  that  thirty  drops 
of  laudanum  equal  one  grain  of  powdered  opium.  What  would  be 
the  effect  of  this  amount  of  opium  upon  a  person  in  good  health  it 
is  impossible  to  state,  for  physicians  do  not  have  occasion  to  give 
opium  to  any  but  persons  suffering  with  disease.  The  doses  named 
have  a  very  decided  effect  in  quieting  pain,  if  it  be  not  too  severe,  and, 
as  has  been  said,  no  symptoms  whatever  of  the  narcotic  effects  are 
produced.  It  is  certainly  desirable  to  have  some  standard  of  dose 
which  shall  be  precise  in  regard  both  to  the  amount  to  be  given  at  a 
time  and  to  the  intervals  between  the  doses.  It  may  be  given  in  the 
manner  that  has  been  described  without  danger  in  all  forms  of  chronic 
or  acute  disease  in  which  its  effects  appear  likely  to  be  useful,  unless 
there  is  evident  reason  to  the  contrary. 

There  have  now  been  mentioned  three  stages  of  chronic  disease, 
and  the  treatment  of  each  of  them  has  been  discussed.  These  stages 
are,  first,  that  in  which  disease  has  progressed  to  an  extreme  limit, 
it  being  evident  that  important  organs  are  organically  changed  and 
life  threatened  with  immediate  extinction.  As  a  type  of  this  was 
mentioned  the  condition  which  is  so  commonly  seen  in  hospital 
practice  in  which  dropsy  and  oppression  are  the  prominent  symp- 
toms. The  second  stage  is  that  form  of  disease  in  which  there  is 
distinct  evidence  of  organic  lesion  but  life  is  not  immediately  threat- 
ened, although  it  is  plain  that  death  must  be  the  consequence  of  a 


THE   TREATMENT   OF   CHRONIC   DISEASE.  221 

great  increase  of  the  disease.  As  a  type  of  this  stage  was  given  the 
account  of  a  man  sixty  years  old  with  intermitting  heart.  The  third 
stage  is  that  form  of  disease  in  which  the  symptoms  are  very  vague, 
it  seeming  as  if  organic  lesion  must  be  already  existent,  although  no 
subjective  evidence  of  it  can  be  discovered,  or  that  organic  lesion  soon 
will  arise  if  the  bad  symptoms  continue.  It  was  said  that  for  this 
stage  of  chronic  disease  it  is  essential  to  endeavor  to  change  the  habit 
of  body,  especially  as  under  the  circumstances  there  is  no  indication 
for  any  more  direct  treatment  or  for  medication.  The  management 
of  this  last  stage  was  less  fully  elaborated  than  that  of  the  other  two, 
and  it  will  be  best,  therefore,  before  closing  the  subject  of  treatment, 
to  make  some  further  statements  in  regard  to  it.  Chronic  disease 
should  be  more  susceptible  to  the  influence  of  good  management  at 
its  beginning  than  when  more  advanced,  for  the  less  the  organic 
change  the  more  likely  is  it  that  a  perfect  cure  can  be  effected,  and  if 
there  is  no  organic  lesion  it  is  required  only  to  effect  a  cessation  of 
the  disordered  state  of  the  organism  to  attain  a  cure.  The  advantages 
of  change  of  climate  were  mentioned,  but  as  that  most  valuable  means 
of  treatment  is  a  special  subject  it  would  be  inadvisable  to  attempt  its 
elaboration  here.  It  was  also  said  that  cure  institutions  and  mineral 
springs,  where  special  systems  of  living  have  been  arranged,  are  often 
most  efficacious  methods  of  changing  the  habit  of  body.  These  sys- 
tems of  treatment  have  been  brought  to  much  greater  perfection  in 
Europe  than  anywhere  in  America,  although  there  is  reason  to  think 
there  are  natural  mineral  springs  in  this  country  which  are  equal  to 
any  to  be  found  elsewhere.  Springs,  however,  have  comparatively 
little  value  unless  their  properties  have  been  long  studied  and  a  sys- 
tem of  life  instituted  at  them  which  places  those  who  seek  treatment 
under  the  care  of  experienced  physicians. 

In  connection  with  the  subject  of  the  treatment  of  chronic  disease 
while  still  in  its  earliest  stage,  there  may  be  mentioned  a  condition 
which  is  very  common  in  civilized  life,  and  which,  if  the  truth  be  told, 
is  even  yet  but  little  understood,  although  it  has  engrossed  a  large 
share  of  the  attention  of  physicians.  It  is  that  state  of  disease  or 
disorder  in  which  an  excess  of  uric  acid  is  found  in  the  urine.  Most 
commonly  uric  acid  is  discovered  in  the  urine  of  persons  who  have 
consulted  a  physician  because  of  headache  or  digestive  disorder,  or 
perhaps  only  of  vague  malaise  without  special  symptom  of  any  kind. 
The  physiology  of  this  curious  condition  is  not  understood,  but  its 
concurrence  with  disordered  digestion  has  been  so  frequently  observed 


222  THE   ORIGIN   OF   DISEASE. 

that  it  is  almost  certain  that  the  two  are  related.  The  clinical  observa- 
tion has  often  been  made  that  uric  acid  will  disappear  from  the  urine, 
and  all  the  uncomfortable  symptoms  that  commonly  accompany  it 
disappear  also,  when  the  patient  has  the  amount  of  his  food  reduced, 
if  he  is  taking  too  much,  or  his  manner  of  living  regulated.  Uric  acid 
lithiasis  often  disappears  completely,  and  the  individual  who  has  been 
affected  with  it  seems  as  well  as  before  the  attack.  On  the  other 
hand,  it  is  not  infrequently  the  precursor  of  chronic  organic  disease, 
and  therefore  it  is  important  in  all  cases  to  endeavor  to  institute  such 
treatment  as  will  cure  it,  which  will  be  most  certainly  accomplished  in 
the  majority  of  cases  by  trying  to  change  the  habit  of  body. 

A  valuable  means  for  accomplishing  a  change  of  the  habit  of  body 
is  the  use  of  milk  diet.  Patients  who  for  any  reason  cannot  have 
change  of  climate  may  often  find  milk  diet  a  good  substitute.  In 
any  of  the  vague  forms  of  chronic  disease  that  have  been  discussed 
in  which  the  existence  of  organic  disease  is  feared,  or  in  which  it  is 
thought  it  will  come  if  not  prevented,  and  no  indications  show  that 
some  particular  treatment  or  any  special  medicine  is  called  for,  milk 
diet  may  be  used.  It  is  often  very  difficult  to  get  middle-aged  or 
older  persons  to  change  their  habits,  and  frequently  such  people  can- 
not go  to  a  European  spring  or  have  a  temporary  change  of  climate. 
Such  persons  can  be  put  upon  an  exclusively  milk  diet  for  six  weeks 
and  still  continue  their  ordinary  vocations,  unless  their  mode  of  life  be 
an  unusually  active  one.  The  quantity  of  milk  necessary  to  be  taken 
daily  is  from  two  and  a  half  to  six  pints ;  delicate  persons  and  women 
often  do  best  with  the  smaller  quantity.  If  two  and  a  half  pints  are 
ordered,  half  a  pint  may  be  taken  at  eight  and  eleven  in  the  morning, 
and  at  one,  four,  and  seven  after  noon.  In  taking  two  quarts  the 
patient  should  be  given  half  a  pint  every  two  hours,  beginning  at  eight 
in  the  morning  and  continuing  until  ten  at  night.  It  is  important  to 
fix  the  amount,  and  the  hours  when  it  is  to  be  taken,  for  if  this  is 
left  to  the  individual  too  much  or  too  little  will  almost  always  be 
taken.  Patients  put  upon  milk  diet  as  a  means  of  treatment  in  the 
manner  described  should  be  kept  to  it  rigidly  for  six  weeks,  and  then 
gradually  go  back  to  the  use  of  ordinary  food.  Persons  upon  milk 
diet  can,  as  has  been  said,  generally  continue  their  vocations,  and  the 
change  of  the  bodily  condition  that  is  effected  by  such  a  revolution  in 
regard  to  food  is  wonderful.  The  change  alone  is  frequently  very 
beneficial  to  the  health,  although,  of  course,  if  the  patient,  as  soon  as 
the  six  weeks  have  passed,  lapses  from  the  milk  diet  to  his  old  habits, 


THE   TREATMENT   OF   CHRONIC   DISEASE.  223 

only  temporary  improvement  can  be  expected  if  the  disease  was  of 
serious  nature.  Another  gain,  however,  is  often  derived  from  milk 
diet,  which  is  that  after  a  patient  has  for  a  period  of  six  weeks  lived 
upon  milk  alone  his  ordinary  ways  of  life  as  well  as  his  habits  of 
body  have  been  so  thoroughly  revolutionized  that  it  is  generally  less 
difficult  to  get  him  to  submit  to  the  rules  of  regimen,  diet,  and  medi- 
cation that  seem  best.  Only  those  who  have  practised  medicine  can 
appreciate  how  difficult  it  is  to  get  patients  to  submit  to  the  simplest 
and  most  palpably  necessary  rules  of  life.  The  things  they  are  told 
to  do  seem  so  simple  that  they  cannot  be  brought  to  believe  them  of 
sufficient  importance  to  take  the  trouble  to  remember  them  and  to 
carry  out  what  they  are  told  must  be  done.  A  man,  however,  who 
has  been  for  six  weeks  upon  milk  diet  is  like  a  field  which  has  been 
ploughed  and  lies  fallow  for  the  seed.  He  does  not  know  exactly 
what  to  eat,  and  he  is  ready  to  be  directed.  The  directions  given  at 
such  a  time  are  likely  to  be  carried  out  for  a  good  while  with  much 
regularity,  although,  of  course,  if  a  watch  is  not  kept  the  patient  will 
probably  fall  back  into  his  old  habits.  Milk  diet  has  been  highly 
recommended  and  much  used  for  hysterical  women,  but  not  so  much 
for  men  and  for  organic  disease  in  the  manner  that  has  been  de- 
scribed. It  must  not  be  thought  for  that  reason  that  it  is  not  a 
powerful  means  to  affect  the  health,  for  it  can  be  beneficial,  when  cor- 
rectly used,  for  men  who  have  been  robust  as  well  as  for  women. 
Thus  milk  diet  may  accomplish  two  important  things :  it  often,  un- 
aided, brings  about  the  desired  change  of  the  habit  of  body;  and  it 
gives  an  opportunity  to  institute  such  rules  of  living  as  seem  necessary 
by  bringing  the  patient  into  a  condition  of  submission,  so  that  he  will 
heed  advice. 

In  the  chapters  dealing  with  the  various  organs  it  was  shown  that  in 
chronic  disease  the  commonest  pathological  lesions  are  fibroid  growth 
and  disease  of  the  blood-vessels,  and  emphasis  was  laid  upon  the  fact 
that  these  conditions  render  tissues  so  changed  specially  liable  to 
inflammation.  Inflammation,  therefore,  which  is  frequently  of  latent 
character,  is  almost  an  essential  part  of  the  ordinary  processes  of 
chronic  disease.  In  dealing  with  questions  of  treatment  it  is  very 
important  to  keep  this  fact  in  mind.  There  cannot  be  two  opinions 
in  regard  to  the  value  of  rest  in  the  treatment  of  most  forms  of  inflam- 
mation. Whenever  in  chronic  disease  there  is  inflammation,  or  even 
strong  reason  to  suspect  its  presence,  it  is  in  most  instances  good 
treatment  to  endeavor  to  keep  the  part  quiet  that  is  inflamed,  or,  if 


224  THE   ORIGIN   OF   DISEASE. 

the  condition  is  a  general  one,  to  procure  rest  for  the  individual,  and 
this  can  generally  be  accomplished  by  putting  him  to  bed.  The  dura- 
tion of  the  rest  must,  of  course,  be  determined  according  to  circum- 
stances. The  importance  of  rest  in  the  treatment  of  chronic  disease 
could  hardly  be  exaggerated.  Those  who  are  chronically  ill  are  often 
allowed  to  drag  themselves  about,  becoming  all  the  time  worse,  when 
so  simple  a  measure  as  going  to  bed  for  a  few  days  would  turn  the 
tide  so  as  to  make  it  set  in  the  direction  of  cure.  It  may  be  laid  down 
as  a  rule  that  during  the  periods  when  there  is  inflammation  in  chronic 
disease  rest  is  indicated. 

It  could  hardly  be  expected  that  after  having  spent  a  large  part 
of  my  professional  life  in  clinical  work  I  should  have  resisted  the  in- 
clination to  write  upon  treatment,  for  it  is  the  most  important  of  all 
subjects  in  medicine,  and  no  one  can  practise  profitably  without  form- 
ing opinions.  That  which  has  been  expressed  has  been  of  necessity 
somewhat  desultory,  for  it  consists  only  of  my  own  views  and  im- 
pressions and  has  been  written  without  any  wish  to  make  a  complete 
treatise  upon  any  of  the  subjects  discussed.  This  has  not  been  because 
I  have  not  formed  definite  opinions  upon  many  and  important  points 
in  regard  to  the  treatment  of  chronic  disease.  The  principal  of  these 
points  are,  first,  that  the  treatment  of  chronic  disease  should  be  ap- 
proached more  hopefully  and  with  greater  confidence  than  is  usual, 
because  so  much  can  be  accomplished  for  its  cure,  or,  if  that  be  im- 
possible, for  its  relief.  Secondly,  too  many  drugs  should  not  be  used, 
as  it  is  reasonable  to  suppose  that  the  number  of  them  that  are  of  real 
value  is  limited.  On  the  other  hand,  it  is  certain  that  the  few  drugs 
whose  beneficial  effects  have  been  established  are  essential  to  enable 
any  one  to  accomplish  the  best  results.  Thirdly,  there  is  no  specific 
treatment  for  chronic  disease,  but  it  must  be  managed  by  common- 
sense  rules,  and  the  best  form  of  treatment  is  that  which  has  been 
called  symptomatic.  As  yet  there  are  few  systems  of  treatment,  but 
more  must  soon  be  established,  and  meanwhile  the  cases  which  are 
vague  and  without  anything  to  show  that  some  particular  treatment 
is  required  are  best  managed  by  trying  to  effect  that  which  has  been 
described  as  a  change  of  the  habit  of  body. 


INDEX. 


Adipose  tissue  in  Bright's  disease,  9. 
Adventitia,  boundaries  of,  38. 

disease  of,  38. 

improper  classification  of,  38. 
Age,  complexity  of  anatomical  structure  in,  10. 

physical  changes  produced  by,  10. 

the  disease  of,  8. 
Albumen  and  casts  in  urine,  significance  of, 

178. 
Amyloid  degeneration  of  kidney,  150. 

disease  of  heart,  79. 

disease,  resemblance  to  fibrosis,  127. 

of  kidney,  132. 

Aneurism,  relation  to  atheroma,  57. 
Aorta,  growths  in,  56. 
Apoplexy,  cause  of,  172. 
Arterial  degeneration,  extreme  development 

of,  55- 

seat  of  origin  of,  56. 
Arteries,  35. 

classification  of,  36. 

histology  of,  36. 
Arterio-capillary  fibrosis,  157. 

Gull  and  Button's  view  of,  38. 
Arteritis  in  infancy,  43. 
Artery,  complete  closure  of  an,  45. 

unusual  form  of  degeneration  of,  46. 
Atheroma,  54. 

relation  to  aneurism,  57. 
Atmosphere  as  a  cause  of  disease,  4. 
Autopsy  in  a  case  of  Bright's  disease,  175. 

B. 

Bile-ducts  in  capsule  of  liver,  114. 

new-formed,  108. 
Blood  in  air-sacs  of  lungs,  96. 
Blood-channels  in  diseased  intima,  54. 
Blood-islands,  49. 
Blood-vessels,  35. 

development  of,  in  embryos,  49. 
in  morbid  tissue,  48. 

disease  of,  in  kidney,  138. 
in  liver,  113. 


Blood-vessels,  displacement  of,  in  kidney,  139. 
in  a  case  of  Bright's  disease,  177. 
in  central  canal  of  spinal  cord,  165. 
in  mucosa  of  colon,  50. 
in  thickened  intima,  53. 
microscopical  examination  of,  35. 
mode  of  growth  of  new,  49. 
of  heart,  63,  81. 
of  lung,  95. 
structure  of  new,  49. 
thickening  of  splenic,  117. 
Brain,  171. 

disease,  prognosis  in,  202. 
syphilis,  172. 
Bright's  disease,  autopsy  in  a  case  of,  175. 

beginning  with  spinal  symptoms,  188. 
fat  in,  9. 

lesions  of  the  cord  in,  160. 
of  the  kidney,  135. 
physical  change  in,  9. 
the  disease  of  age,  13. 
the  organ  first  to  be  attacked  in,  187. 
Brown  atrophy  of  heart,  73,  79. 
Buhl's  view  of  phthisis,  25. 

C. 

Calcareous  deposit  in  infant's  kidney,  132. 
in  kidney,  141. 
in  lungs,  99. 
Cancer,  cause  of,  18,  20. 

fibrosis  in,  21. 

vascular  disease  in,  21. 
Cancerous-like  growth  in  kidney,  143. 
Capillaries,  60. 

difficulty  of  study  of,  60. 

disease  of,  in  heart,  67. 

distribution  of,  in  heart,  64. 

in  muscular  fibres  of,  heart,  65,  73. 

in  thickened  arteries,  46. 

narrowing  of,  in  heart,  67. 

of  heart,  64. 

ramification  of,  in  heart,  74. 

seal-ring  appearance  of,  65. 
Capsules,  effusions  beneath,  97. 

225 


226 


INDEX. 


Capsules,  thickening  of  splenic,  116. 
Cardiac  irregularity,  prognostic  value  of,  202. 
Cause  of  disease,  atmosphere  as  a,  4. 
Cell-nests  in  fibroid  lung,  95. 
Cells,  changes  in,  after  death,  124. 

nests  of,  59. 

Central  canal  of  cord,  blood-vessel  in,  165. 
changes  in,  164. 
enlargement  of,  165. 
Cerebral  meningitis,  172. 
Cerebritis,  172. 
Charcot's  cirrhosis,  107. 
Chronic  disease,  diet  in,  216. 
dosage  in,  217. 
mineral   spring  waters  in  treatment 

of,  221. 

prognosis  in,  200. 
rate  of  progress  of,  200. 
stages  of,  221. 
the  essential  pathological  change  in, 

20. 

synovitis,  nature  of,  12. 
Clark,  Sir  Andrew,  27. 
Classification  of  disease,  3. 

difficulty  of,  33. 
Clots,  connection  with  tissue,  57. 

effects  produced  by  shrinking  of,  57. 
formation  of,  in  vessels,  57. 
Colon,  ulcer  of,  126. 
Confusion    of   speech    as   an    indication  of 

chronic  disease,  194. 
Consumption,  22. 
bacilli  in,  100. 
external  causes  of,  30. 
influence  of  heredity  upon,  30. 
Laennec's  view  of,  26. 
lesions  of,  100. 
Niemeyer's  three  forms  of,  24. 

view  of,  23. 

non-infectiousness  of,  28. 
origin  of,  23. 

Sir  Andrew  Clark's  view  of,  27. 
unreasonableness  of  bacillary  origin,  27. 
Contagious  diseases,  31. 
Contracted  kidney,  its  associated  lesions,  13. 

other  organs  involved  in,  19. 
Cord,  spinal  (see  Spinal  cord),  155. 
Coronary  arteries,  obstruction  of,  42. 
Cystic  degeneration  of  heart-muscle  fibres,  70. 
Cysts,  76. 

in  heart,  75. 

in  kidney,  2,  147. 

in  nutmeg  liver,  103. 


Cysts  of  liver,  106. 

of  spinal  cord,  158. 
of  spleen,  119. 

D. 

Death,  causes  of,  96. 

physiological,  15. 
Decay,  physiological,  17. 
Diagnosis,  173. 

errors  of,  193. 

of  a  case  of  Bright's  disease,  174. 

of  enlarged  heart,  179. 

of  heart  disease,  178. 

Diarrhoea,  significance  of,  in  the  aged,  193. 
Diet  in  chronic  disease,  212,  216. 
Digitalis,  dose  to  be  given  for  a  long  time, 
219. 

effects  of  large  doses,  217. 
Disease,  difficulty  in  classifying,  33. 

of  age,  8. 

spontaneous  generation  of,  34. 
Dosage  in  chronic  disease,  217. 
Drugs,  the  use  of,  in  chronic  disease,  209. 

E. 

Ecchymoses  beneath  capsules,  97. 
Effusion  of  blood  beneath  capsules,  97. 
Emphysema,  appearances  of  pulmonary,  91. 

imitated  by  diseased  kidney,  136. 

pulmonary,  89,  98. 
Endarteritis  deformans,  61. 

early  stage  of,  42. 

obliterans,  40. 

syphilitic,  61. 

Environment,  influence  on  disease,  14. 
Epistaxis  as  an  indication  of  chronic  disease, 

194. 
Exercise  in  organic  heart  disease,  214. 

in  treatment  of  heart  disease,  215. 

F. 

Fat,  disease  of,  in  heart,  68. 

in  the  intestine,  127. 

significance  of,  9. 
Fatty  infiltration  of  heart,  82. 
Fibroid  kidney,  134. 

general  characteristics  of,  151. 
Fibroma  on  splenic  capsule,  116. 
Fibrosis  in  youth,  14. 

of  kidney,  136. 

of  Malpighian  bodies,  137,  145. 

of  medulla  of  kidney,  142. 


INDEX. 


227 


Fibrosis  of  peripheral  nerve,  161. 
of  perirenal  fat,  136. 
of  spinal  cord,  161. 
of  spleen,  117. 
of  what  it  consists,  20. 
pulmonary,  89. 
resemblance  to  rheumatism  of  the  aged, 

ii. 

the  disease  of  age,  13. 
Fibrous  tissue,  at  birth,  8. 
in  the  embryo,  8. 
morbid  increase  of,  9. 
Food,  influence  on  disease,  14. 
Fragmentation  of  heart-muscle,  80. 

G. 

Giant  cells  in  consumption,  100. 
Gout,  relation  to  Bright's  disease,  197. 
Growth  resembling  cancer,  21. 

H. 

Habit,  influence  on  disease,  14. 
Habit  of  body,  207. 
Heart,  63. 

amyloid  disease  of,  79. 

anatomy  of,  63. 

blood-vessels  of,  63. 

brown  atrophy  of,  79. 

capillaries  in  muscular  fibres  of,  73. 

capillaries  of,  64. 

compensatory  hypertrophy  of,  84. 

cross-sections  of,  65. 

diagnosis  of  enlargement  of,  179. 

difference  between  young  and  old,  77. 

disease  of  fat  in,  68. 
of  nerves  of,  79. 

distortion  of  fibres,  78. 

fat  layer  of,  82. 

fatty  infiltration  of,  82. 

fibrosis  of,  67. 

fragmentation  of,  80. 

function  of  return  vessels  in,  66. 

hollow  muscular  fibres  in,  69. 

hypertrophy  of,  86. 

peculiarity  of  the  blood-vessels  of,  63. 

structure  of  return  vessels  in,  66. 

valvular  disease  of,  84. 
Heart  disease,  diagnosis  of,  178. 

exercise  in  treatment  of,  215. 
rest  in  treatment  of,  215. 
Hemorrhage,  cause  of  bronchial,  26. 
Heredity,  influence  of,  in  consumption,  30. 
High  tension  pulse,  196. 
Hospitals  as  fields  for  study,  5. 


Humphrey,  G.  M.,  on  physiological  death,  15. 

Hydronephrosis,  148. 

Hypertrophic  cirrhosis  of  liver,  107. 

Hypertrophy  of  heart,  84. 

Hypertrophy  of  muscularis,  a  degeneration,  39. 

I. 

Infancy,  mortality  in,  5. 

Insanity,  lesions  connected  with,  171. 

Intestines,  126. 

amyloid  disease  of,  127. 

cystic  degeneration  of,  126. 

fatty  condition  of,  127. 
infiltration  of,  128. 

Intima,  effects  of  thickening  upon  blood-cur- 
rent, 41. 

irregularity  of  thickening  of,  41. 

puckering  of,  41. 

thickening  of,  37. 
Intravascular  blood  pressure,  196. 

K. 

Kidney,  130. 

amyloid  degeneration  of,  150. 

disease  of,  132. 

vessels  in,  149. 
Bright's  disease  of,  135. 
calcareous  deposit  in,  141. 

in  infants,  132. 

cancerous-like  growth  of,  143. 
changes  in,  produced  by  age,  u. 
condition  of,  in  infancy,  130. 
cysts  in,  147. 

deposit  of  mineral  matter  in.  141. 
disease  of  blood-vessels  of,  138. 
displacement  of  blood-vessels  in,  139. 
early  fibrosis  of,  132. 
extreme  fibrosis  of,  138. 
fibrosis  of,  134,  136. 

of  medullary  portion  of,  142. 
general  characteristics  of  fibroid,  151. 
irregular  contraction  of,  140. 
narrowed  tubule  in,  140. 
relation  to  Bright's  disease,  177. 
shredding  of  capsule  of,  146. 
vascular  disease  of,  133. 
vessels  penetrating  capsule  of,  132. 
Koch's  bacillus,  27. 

L. 

Laennec's  cirrhosis  of  liver,  no. 

view  of  consumption,  26. 
Lesions  in  a  case  of  Bright's  disease,  176. 
Liability  to  disease  in  early  life,  5. 


228 


INDEX. 


Limits  of  life,  8. 
Liver,  102. 

bile-ducts  in  capsule  of,  114. 

Charcot's  cirrhosis  of,  107. 

cirrhosis  of,  112. 

cystic  degeneration  of,  106. 

difference  between  young  and  old,  102. 

disarrangement  of  cells  in,  113. 

disease  of  blood-vessels  of,  113. 

fibrosis  of,  112. 

framework  of,  112. 

hypertrophic  cirrhosis  of,  107. 

Laennec's  cirrhosis  of,  no. 

microscopical  appearances  of  nutmeg,  103. 

nutmeg,  102. 

peculiarities  of  cells  in  disease,  114. 

physical  examination  of,  183. 

relationship  of  lesions  of,  105. 

thickening  of  capsule,  in. 

vacuoles  in  cells,  113. 
Longevity,  influence  of  injuries  on,  12. 
Lungs,  88. 

calcareous  deposit  in,  99. 

diagnostic  indications  of  disease  of,  179. 

effusion  of  blood  into,  96. 

emphysema  of,  89. 

fibrosis  of,  89. 

inflammation  of,  98. 

liability  to  disease,  88. 

pigmentation  of,  99. 

M. 

Malignant  disease,  cause  of,  18. 

resemblance  to  fibrosis,  19. 
Malpighian  bodies,  arrangement  of,  in  infancy, 

130- 

fibrosis  of,  137,  145. 
loops,  amyloid  disease  of,  133. 
Man,  his  environment,  14. 
Mitral    valve,    newly    formed    blood-vessels 

in,  52. 
Meningitis  and  tuberculosis,  169. 

cerebral,  172. 
Metastasis,  121. 

of  malignant  disease,  19. 
Miliary  tubercle,  meaning  of  the  term,  24. 
Milk  diet,  in  chronic  disease,  222. 
in  uric  acid  lithiasis,  222. 
Mineral  springs,  in  treatment  of  chronic  dis- 
ease, 221. 
Molluscum  fibrosum,  resemblance  to  cancer, 

22. 
Morbid  fibrous  tissue,  character  of,  10. 


Mortality  in  infancy,  5. 

Muscle  development,  85. 

Muscular  fibres,  separation  of,  in  heart,  67. 

tenuity  of,  75. 
Muscularis,  disease  of,  38. 

penetrated  by  a  blood-vessel,  53. 

thickening  of,  39. 
Myelitis,  chronic,  162. 

frequency  of,  in  meningitis,  170. 

N. 

Names  of  lesions,  inadequacy  of,  55. 
Nerves  of  heart,  disease  of,  79. 
New  blood-vessels  in  new  tissue  in  adherent 
pericardium,  51. 

in  pericardium,  51. 

peculiar  cells  in,  52. 
New-formed  bile-ducts,  108. 
Niemeyer's  view  of  consumption,  23. 
Nutmeg  liver,  102. 

microscopical  appearance  of,  103. 

O. 

Opium,  dose  of,  219. 
Origin  of  arterial  degeneration,  56. 
of  disease,  18. 

extrinsic  and  intrinsic,  2. 
influence  of  early  attacks  upon,  6. 

P. 

Pain  on  percussion,  significance  of,  in  lung 

disease,  181. 

Pericardium,  obliteration  of,  69. 
Perineal  fat,  fibrosis  of,  136. 
Peripheral  nerve,  fibrosis  of,  161. 
Pigment  in  cardiac  muscular  fibres,  66. 
Pigmentation  of  lungs,  99. 
Plicated  membrane,  destruction  of,  44. 

double,  46,  53. 
Pleura,  thickening  of,  93. 
Pleural  effusion,  physical  signs  of,  181. 
Pneumonia,  98. 

diagnostic  signs  of,  182. 
Private  practice  as  a  field  for  study,  4. 
Prognosis  in  brain  disease,  202. 
in  chronic  disease,  200. 
value  of  examination  of  heart  and  lungs 

in,  203. 

of  urine  analysis  in,  201. 

Protoplasmic  processes  of  developing  capil- 
laries, 54. 

Pulp-sinuses  in  spleen,  121. 
Pulse,  high  tension,  45. 


INDEX. 


229 


R. 

Radial  artery,  disease  of,  45. 
Relation  of  youth  to  age,  6. 
Rest  in  treatment  of  chronic  disease,  224. 

of  heart  disease,  215. 
Rheumatism  of  the  aged,  n. 

relation  of  acute  and  chronic,  12. 


Sarcoma,  cause  of,  18. 

resemblance  to  inflammation,  21. 
Scars,  the  result  of  inflammation,  13. 
Slight  paralytic  symptoms,  cause  of,  195. 
Spinal  cord,  155. 

bony  plates  in,  168. 

chronic  degeneration  of,  162. 

commonest  disease  of,  157. 

cyst  of,  158. 

destruction  of  fibres  of,  161. 

disarrangement  of  fibres  of,  160. 

dropsy  of,  162. 

fibrosis  of,  161. 

frequency  of  pathological  change  of, 

156. 

in  typhoid  fever,  167. 
lesions  of,  in  Bright's  disease,  160. 
necessity  for  microscopical  examina- 
tion of,  155. 

secondary  degenerations  of,  158. 
thickening  of  trabeculae,  159. 
disease,  a  case  of,  188. 
Spleen,  116. 

acute  hypersemia  of,  121. 
contents  of  cysts  in,  120. 
cystic  degeneration  of,  120. 
cysts  in,  119. 
fibrosis  of,  117. 
folding  of,  118. 
morbid  changes  in,  116. 
origin  of  cysts  in,  119. 


Spleen,  physical  examination  of,  183. 

thickening  of  blood-vessels  in,  117. 
of  capsule  of,  116. 

tumor  in  capsule  of,  116. 
Spontaneous  generation  of  disease,  34. 
Stomach,  123. 

difficulty  of  studying  disease  of,  123. 

disease  of  mucous  coat  of,  125. 

thickening  of  pyloric  end  of,  125. 
Sutton,  H.  G.,  29. 
Syphilis,  mode  of  origin  of,  30. 

morbid  fibrous  tissue  in,  31. 
Syphilitic  endarteritis,  61. 
Syringomyelia,  158. 

T. 

Tissues  in  early  life,  6. 

in  the  aged,  6. 

Toadstool  growth  in  artery,  57. 
Treatment  of  chronic  disease,  205. 
rest  as  a  means  of,  224. 

of  a  case  of  digitalis  poisoning,  218. 
Tubercle,  miliary,  24. 
Tubercular  arteritis,  58. 
Tuberculosis,  23. 
Tumor  in  capsule  of  spleen,  116. 

U. 

Uric  acid  lithiasis,  222. 

treatment  of,  222. 
Urine,  failure  of,  to  indicate  kidney  disease, 

191. 
significance  of  albumen  and  casts  in,  178. 

V. 

Vacuolation  of  heart  muscle-fibres,  69. 

of  liver  cells,  113. 
Valvular  heart  lesions,  84. 
Veins,  58. 

disease  of,  59. 
Vena  cava,  disease  of,  59. 


THE   END. 


14  DAY  USE 

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